Hormesis Part 2: Flawed Research and Harmful Misapplications (Including Ketogenic Diets, Intermittent Fasting, Calorie Restriction, and More)

This article is quite a bit longer and more complex than most of my articles. If that doesn’t sound like your cup of tea, check out my other articles here.

In Part 1 of this article series, we outlined the basics of hormesis and how it relates to stress and adaptation. In this article, we’re going to dig into the research supporting hormesis and identify its major flaws. We’ll also take a look at the many misapplications of this erroneous concept, including ketogenic diets, intermittent fasting, caloric restriction, and more.

Flaws In The Research

As I mentioned in Part 1 of this series, most of the research supporting the original view of hormesis was based on particular benefits seen in response to low doses of toxic chemicals.  But when all the data was looked at, it was found that these “benefits” came at the cost of harm elsewhere.

There were several other issues with this earlier research, including various methodological issues, conflicting data from different studies, and conflating stimulation or adaptation with health benefits (1, 2, 3).

As for the newer definition of hormesis (the idea that small amounts of stress are beneficial to our health because they improve our body’s defenses, and that this stress is responsible for the health benefits of virtually all aspects of our environment), there’s a plethora of research to dig into.

One of the most commonly cited areas of research in support of this version of hormesis is caloric restriction.

It’s known that caloric restriction causes stress, and it’s also known that caloric restriction increases lifespan. So, those in favor of hormesis suggest that the stress caused by caloric restriction must be responsible for the increases in lifespan.

However, it’s clear that the benefits of caloric restriction aren’t due to the stress caused by the restriction of calories and are rather due to the restriction of particular amino acids, the restriction of PUFA, and poor study design, as I explained in this article. The reduction in endotoxin production also plays a major role in the benefits of caloric restriction and is independent of the stress caused by this intervention (4).

There are also issues with the various organisms used to study effects on lifespan, and these issues confound much of the research on lifespan extension beyond caloric restriction.

C. elegans, for example, are worms that are often used for these studies, but the extension of lifespan seen in this organism is accomplished by shifts toward or entry into a hibernation state called dauer rather than improvements in health (5).

The dauer state is activated by stress, which could be caused by things like a lack of food (caloric restriction) or overcrowding, and results in several metabolic changes: fat becomes heavily favored as a fuel over glucose, the activity of the Krebs cycle and electron transport chain is substantially decreased, and the metabolic rate is largely reduced (5). In this state, C. elegans also has much greater stress resistance.

However, this state doesn’t represent a viable, healthy state in a normal environment:

It is important to note that the increased reliance on these alternative pathways can often result in energetically crippled, albeit long-lived animals. Mitochondrial-based metabolism and the TCA cycle presumably evolved in large part because of the ability to produce the most ATP molecules per unit of nutrient consumed. Reducing an organism’s reliance on such pathways may allow a worm to survive for an extended period of time in the controlled laboratory environment but would probably place this animal at a significant disadvantage in the real world, where only the fastest and reproductively fittest survive.” (5)

In a little bit, we’ll see that these adaptations to stress in C. elegans also happen to be mirrored in us humans.

Other studies have noted various other differences between C. elegans and other species, including that they’re resistant to extraordinarily high levels of superoxide and exhibit unique lifespan extension in response to various toxins that isn’t seen in other species (6).

In other words, just because certain interventions extend lifespan in C. elegans doesn’t mean they improve the health of C. elegans or that they would improve the health of other organisms. In fact, the extreme metabolic impairment that accompanies this lifespan extension would suggest the opposite.

In addition to life extension, there are several other adaptations to stress that are considered to be beneficial and are cited in support of hormesis, including autophagy, mitophagy, mitochondrial biogenesis, uncoupling, and resistance to oxidative stress, among others.

And, the activation of many of the signals that lead to these adaptations are also considered to be beneficial, including AMPK, Nrf1 and Nrf2, sirtuins (SIRTs), PGC-1α, PPAR-α, PPAR-­γ, nitric oxide, and others, as well as the increased secretion of stress hormones like adrenaline (epinephrine) and cortisol.

But to evaluate whether these effects are truly beneficial, we have to begin at the origin of the stress adaptation cascade: reactive oxygen species.

Reactive Oxygen Species and Adaptation

Reactive oxygen species, or ROS, are highly reactive molecules that are normally produced in small amounts in the mitochondria as a byproduct of energy production. The production of ROS is increased during stress and also as a direct result of various damaging factors, like radiation and lipid peroxides.

The increased production of ROS has historically been considered harmful, as it’s a primary cause of cellular damage. The downstream effects of ROS include damage to proteins, lipids, and DNA, which can lead to cell death and are implicated in virtually all chronic diseases.

However, the role of ROS in the adaptive response has been elucidated more recently and has shifted the general sentiment towards a more positive light.

It’s been shown that ROS are necessary for many of the signaling functions that allow for adaptation, which includes adaptive responses like uncoupling, autophagy, and mitochondrial biogenesis, as well as the activation of heat shock protein, apoptosis, JNK and other inflammatory pathways, hypoxia inducing factor (HIF), and others (6, 7, 8, 9, 10, 11, 12, 13, 14, 15, 16, 17, 18, 19).

Simply put, ROS are integral to the adaptive process.

And, the adaptive processes stimulated by ROS production are vital to our health. So, it’s not surprising that dysfunction in these adaptive pathways is implicated in aging and various diseases.

For example, reductions or defects in autophagy have been implicated in obesity, type 2 diabetes, neurodegenerative diseases like Parkinson’s and Alzheimer’s, rheumatoid arthritis, cardiovascular disease, cancer, liver disease, and other degenerative conditions (20, 21, 22, 23, 24, 25, 26, 27, 28). And, lower levels of uncoupling are associated with decreased lifespans (29).

So, based on these findings it’s assumed that increasing the stimulation of these adaptive processes, like uncoupling, autophagy, and mitochondrial biogenesis, by increasing ROS production will reduce aging and degeneration.

This has led to the supposition that hormetic interventions like ketogenic diets, caloric restriction, and exercise, which increase ROS production and cause stress, are beneficial by causing these adaptive downstream effects.

In other words, the entire model of hormesis hinges on the idea that stimulating adaptive responses, typically by increasing ROS production, is beneficial.

But this is a textbook example of the reductionist view of adaptation I explained in Part 1 of this series.

There’s no denying that ROS stimulate adaptive defensive reactions to better deal with whatever challenge is presented to the organism. And, assuming continued stress, this adaptation is always going to be better than less adaptation or no adaptation at all because it better suits the organism to deal with exposure to these stressors.

But that doesn’t mean that stimulating the production of ROS and the downstream adaptive processes is inherently beneficial for the organism.

In fact, increased levels of ROS are seen in aging and degenerative conditions, suggesting that exposing ourselves to factors solely on the basis of increased ROS production and the stimulation of adaptive responses is misguided, to say the least (5, 13, 30, 31, 32, 33, 34, 35, 36, 37, 38, 39, 40, 41, 42, 43, 44, 45, 46, 47, 48).

And, considering that there are reductions or defects in the adaptive processes like autophagy and uncoupling in these conditions despite the increased levels of ROS, increasing the production of ROS via stress to improve these conditions certainly doesn’t make much sense.

To explore this concept further, let’s consider the energetic contexts when ROS may be produced.

Reactive Oxygen Species and Energy

ROS and The High Energy State

The first situation when ROS are produced beyond typical levels would be the high-energy state. This state is the result of uninhibited energy production, where mitochondrial respiration functions efficiently and rapidly. As ATP levels rise relative to ADP, electrons build up at the electron transport chain, which then increases the production of ROS (5, 49, 50).

This ROS production then stimulates processes like mitochondrial biogenesis and autophagy, which improve our capacity for energy production and act as cellular repair processes. In this context, these adaptive processes would positively contribute to the health of the organism as a whole.

Then, in order to stop the continual production of ROS (which we know can be damaging), uncoupling occurs, which drastically reduces the production of ROS and also typically reduces the production of ATP. In this case, the reduced production of ATP isn’t an issue considering that a high level of ATP is what led to the ROS production in the first place.

It’s also important to note that in this scenario, the high-energy state of the cell (which involves both high ATP and high CO2), is protective against the ROS produced, preventing damage from occurring (51, 52, 53, 54, 55, 56).

Now let’s consider another situation where ROS are produced: the low-energy stress state.

ROS and The Low-Energy Stress State

ROS may be produced in this state for several reasons. They may be produced as a direct effect of damaging factors such as radiation or lipid peroxides, or they may be produced due to the inhibition of the function of the electron transport chain (or energy production) by factors like endotoxin, nitric oxide, lipid peroxides, PUFA metabolites, resveratrol, methylmercury, hypoxia, excess lactate, or a high FADH2/NADH ratio (57, 58, 59, 13, 60, 61, 62, 63, 64, 65, 66, 67, 68, 69, 70, 12, 71, 72, 73, 74, 75, 76, 77, 78, 79).

(Note: A high FADH2/NADH ratio occurs during excessive fat oxidation, which occurs during low-carb or ketogenic diets and fasting/starvation, as I detailed in this article.)

And, ROS produced in this context have many of the same effects, in this case characterized as defensive reactions. They stimulate processes like mitochondrial biogenesis and autophagy/mitophagy, which improve the organism’s ability to deal with future stressors (13, 57, 60, 62, 76, 77, 78, 79). And they also cause uncoupling in order to stop the continual production of ROS from the electron transport chain and the resulting damage that would occur (70, 78, 80, 81, 82, 83).

But in this scenario, the cellular energy state is low due to both the inhibited electron transport chain function and the subsequent uncoupling. This leaves the cell susceptible to oxidative damage from the ROS produced and also stimulates the production of stress hormones in order to supply fuel to the cell and drive energy production (84, 85, 86). This stress hormone production is acknowledged by those in favor of hormesis and is even considered to play a role in the “beneficial” hormetic effects (78, 87, 88).

Additionally, this low-energy uncoupled state promotes the Warburg effect, which is seen in cancer cells (89, 90, 91). In this situation, ATP can’t be produced at the electron transport chain due to the uncoupling and therefore must be produced by glycolysis.

To summarize, ROS in the low-energy stress state cause the same mitochondrial biogenesis, autophagy, and uncoupling as ROS in the high-energy state. But, because of the lack of energy, the cell is susceptible to damage by these ROS and stress hormones are released to supply fuel and drive energy production.

These stress signals cause a cascade of anti-metabolic effects, such as the inhibition of thyroid, reproductive, immune, and digestive function, which I’ve described in this article. Altogether, these effects parallel the dauer hibernation state seen when C. elegans experience stressful environments, where the conservation of energy and improved stress tolerance come at the cost of function.

So, it’s clear that the effects of ROS production are dependent on the energetic context. And, adaptations to ROS produced in the high-energy state are beneficial whereas adaptations to ROS produced in the low-energy stress state result in a cascade of harmful effects.

In support of this idea, it’s been suggested that the decoupling of ATP production and ROS production, or the production of ROS without adequate ATP production (which would be the low-energy stress state), is responsible for neurodegenerative conditions (44, 45). Additionally, it’s been shown that ischemia/reperfusion injury, neuronal excitotoxicity, and necrosis are caused by high ROS and low ATP (92, 93, 94), and this low-energy, high ROS state is also seen in aging, hypoxia, and insulin resistance (30, 40, 43, 46, 51, 95, 96).

So, contrary to the ideas put forth by those in favor of hormesis, just because ROS production may result in beneficial adaptive effects does NOT mean that increasing ROS or its downstream adaptive effects, like autophagy and mitochondrial biogenesis, even in non-excess, is inherently beneficial! We must consider the mechanism behind the production of ROS – whether it’s driven by a high energy state or by inhibited respiration and/or direct damage – in order to determine the effects.

When considering the organism as a whole, ROS production in the low-energy stress state leads to the conservation of energy and reduced complexity, which is largely mediated by the stress hormones. And if this continues chronically, it results in the degenerative states characterized by elevated ROS and low energy.

So at best, the hormesis research suggests that stress builds tolerance to stress and that, rather than improving our health, this stress tolerance reduces our ability to function on a high level.

To quickly summarize, stressors and damage that drain the energy pool and increase ROS production result in adaptations that are NOT ideal for the long-term health of the organism.

But, none of this is to say that there aren’t beneficial effects from factors that cause stress.

Weighing Specific Effects and Stress: Exercise, Intermittent Fasting, and Low-Carb & Ketogenic Diets

Considering that every factor results in some amount of energy usage, meaning that everything is a potential stressor, the fact that there are beneficial effects from stressors really goes without saying. But, in order to provide contrast with the idea that the benefits of these factors are derived from adaptations to the stress they cause, let’s break down a few examples.

Hormesis and Exercise

First let’s consider exercise. There are, without a doub­­t, beneficial effects of exercise. And, of course, exercise is a stressor, as it requires energy and can therefore cause stress. But, does that mean the benefits of exercise are due to the stress it causes?

Those in favor of hormesis argue that this is the case – that the stress from exercise results in adaptations that account for its beneficial effects. And this is even common to hear from those in the fitness industry – they’ll say that damaging or stressing our muscles is what causes the beneficial adaptations that lead to improved health. But, there’s considerable evidence against this position.

First is that walking and other leisurely activity has been shown to be massively beneficial compared to being sedentary, which has been shown to be detrimental independent of periods of intense physical activity (97, 98, 99, 100, 101, 102). In other words, inactivity throughout the day has been shown to harm our health and even intensely stressful physical activity during isolated instances (like working out) doesn’t make up for this sedentarism.

Additionally, when compared to more intense exercise, the benefits of leisurely activity have been shown to be much greater in proportion to the amount of stress caused, suggesting that aspects other than stress are responsible for the benefits of light activity (97, 98).

Second is that the benefits from different types of exercise can vary while the amount of energy used is the same, as is shown in various isocaloric exercise interventions (103, 104, 105, 106, 107). This suggests that the specific effects of exercise, like putting tension on the musculofascial system, must account for at least some of the benefits of exercise rather than the energy expended and resulting stress caused.

Third is that muscle growth, or hypertrophy, is more tightly related to mechanical loading rather than muscular stress or damage (108). And, hypertrophy in response to greater stress and damage appears to differ from hypertrophy in response to greater muscular tension (109).

Stress and damage appear to cause greater sarcoplasmic hypertrophy, which is an increase in protein content of the sarcoplasm that doesn’t contribute as much to muscular strength. This hypertrophy represents increases in resources within the cell, which improves the muscle’s ability to handle future stress.

This is contrasted with myofibrillar hypertrophy, which is an increase in the amount of myofibrillar protein in the muscle cell. An increase in these structural components enhances muscular strength and occurs in response to greater muscular tension with less stress and damage.

All of this suggests that while exercise does cause stress that leads to adaptation, it’s the specific effects, rather than the stressor effects, that are responsible for its benefits.

As an aside, it’s also worth mentioning that neither type of muscle growth is inherently beneficial. When considering the organism as a whole, muscle is very energetically expensive. So, excessive muscle mass can waste energy that would better be used by other areas of the body (like the brain), and therefore isn’t always ideal for our health.

Hormesis and Intermittent Fasting

We can look at intermittent fasting as a second example for which hormesis is cited as the reason for its benefits.

Intermittent fasting often takes the form of eating only within an 8-hour window and fasting during the other 16 hours of the day. In other words, intermittent fasting is simply a lack of food for an extended period of time.

The most noteworthy effects of intermittent fasting are therefore twofold:

  • Immense stress caused by an acute lack of food (110, 111), and
  • A reduction in gut irritation, because if we aren’t eating any food then any gut irritation would be drastically reduced

This lack of gut irritation is certainly beneficial (although it can be accomplished through other, less-stressful means), whereas the stress caused by the lack of food is quite harmful. And the final outcome of intermittent fasting would be determined by weighing these two effects against each other.

However, these two effects are often conflated.

If someone is experiencing benefits from intermittent fasting, it likely means that the benefits of reducing gut irritation are outweighing the stress of not eating. This is relatively common, as gut irritation (and the production of endotoxin and other toxic factors that comes with it) is one of the most universal and damaging issues we face in our modern world and can therefore outweigh the stress caused by a lack of food.

Those in favor of hormesis, however, attribute the benefits of intermittent fasting to the stress itself rather than the beneficial reduction in gut irritation. But, it’s now been shown that the beneficial effects of caloric restriction are due to the decrease in gut irritation and endotoxin production, not the adaptations to the stress caused by a lack of food, and the same is likely true of fasting (4).

While it may go without saying, because of the stress caused by not eating, the benefits of reduced gut irritation would be better achieved by improving gut function and reducing the consumption of irritating, hard-to-digest foods rather than intermittent fasting.

(For a more in-depth exploration of the harmful effects of fasting, check out this article)

Hormesis and Low-Carb, Ketogenic, and Carnivore Diets

The same can be said for low-carb, ketogenic, and carnivore diets, which mimic the fasted state (also called the starvation state). Like fasting or starvation, these diets cause considerable amounts of stress (112, 113, 114; this is also explained more thoroughly in these articles). And under the guise of hormesis, this stress is considered to be responsible for the benefits seen.

But, like fasting, the benefits from these diets can largely be attributed to reductions in gut irritation rather than stress because many of the irritating, hard-to-digest foods that would lead to increased endotoxin production are carbohydrates, and these types of foods are avoided on these diets. This has been supported by recent evidence showing that the anti-seizure benefits of ketogenic diets are due entirely to their effect on the gut and rather than the stress they cause (115).

The examples detailed in this section have supported that it’s the specific effects of stimuli that are responsible for any health benefits seen, not stress or damage. And remember, because energy consumption is a universal phenomenon between all stimuli, if stress or damage were responsible for the benefits of these factors, then the argument would have to be made that the stress caused by any factor, including things like ionizing radiation, psychological stress, and heavy metal exposure, is beneficial.

This brings us to the final feature of hormesis that needs to be addressed: the U-shaped curve.

All You Need Is… Stress?

As I mentioned in Part 1 of this series, the definition of hormesis is expanding, and not for the better. Anything that follows a U-shaped dose-response, meaning that it can be harmful at a low dose, beneficial at a moderate dose, and harmful again at a high dose, is now considered to be hormetic.

By disguising the idea of hormesis behind the U-shaped curve, it’s allowed those in favor of hormesis to suggest that virtually all environmental factors are hormetic, meaning that the benefits of all factors are attributed to adaptations to the stress or damage they cause.

It’s reached the point where the benefits from things like essential vitamins and minerals (sodium, potassium, calcium, iron, copper, zinc, vitamins A, C, and E, etc.) and even water are considered to be a result of hormesis because they follow this U-shaped curve (88, 116, 117, 118, 119).

And there’s no question that many of these factors do fit the U-shaped dose-response:

  • Exercising too little is harmful, a moderate amount of exercise is beneficial, and exercising too much is harmful
  • Drinking too little water is harmful, drinking enough water is beneficial, and drinking too much water is harmful
  • And consuming too little zinc is harmful, consuming enough zinc is beneficial, and consuming too much zinc is harmful

But just because they fit the U-shaped dose-response and can also cause stress does NOT mean that these factors are beneficial because they cause stress.

Yet that’s what’s being suggested.

Through its association with the U-shaped dose-response curve, hormesis has essentially become the idea that the only way to improve function is to cause stress or damage (which happens to support many modern medical interventions, industrial chemical and radiation exposure, and our terrible food supply and farming practices).

And, quite frankly, the definition had to expand in this way in order for hormesis to appear to be a viable concept. If it’s recognized that the benefits of factors that follow the “hormetic” U-shaped dose-response aren’t due to the stress they cause, it would have to be acknowledged that effects other than stress are responsible for the benefits of our environmental inputs, and eventually, that stress itself is harmful.

So instead, we’re left with the ridiculous notion that stress is the only way to improve health and function.

For example, this study in support of hormesis suggests that water, vitamins, and cognitive stimulation are hormetic factors (116).

But this is utter nonsense! To suggest that these factors are hormetic would mean that in their ideal, most beneficial doses, they cause stress which leads to adaptations that account for their benefits.

I don’t know about you, but to me, suggesting that the proper amounts of essential nutrients like water and vitamins and minerals are beneficial because they cause stress, rather than because they supply a vital nutrient that’s required for us to properly function, is simply ridiculous, if not entirely illogical.

They even suggest that intellectual activities, such as those examined in this study, are beneficial for the brain due to their hormetic effects (120). But, the study they cited shows that increased leisure activity and cognitive stimulation, such as reading magazines and playing bingo or card games, are beneficial for the brain.

To suggest that these activities are stressful enough to be hormetic is nonsensical, especially when these are the same people saying that caloric restriction and substantial amounts of exercise, which are both considerably stressful, fall in the same hormetic dose range. By this same reasoning, simply standing in place or typing on a keyboard would be stressful enough to be hormetic, so why would we need exercise anyway?

As you can see, by the logic of this new definition of hormesis, literally any environmental factor that we adapt to, which is all environmental factors, is hormetic.

They’ve muddied the waters so much that “hormesis” has become synonymous with “adaptation,” allowing them to suggest that because water and cognitive stimulation are beneficial, ionizing radiation, dangerous heavy metals, and other toxic factors must be as well.

This absurdity leads us to the final major flaw in the concept of hormesis, and specifically its relationship with the U-shaped curve: stress is cumulative.

As I explained in Part 1, stress is a universal response to an energy deficit. And, because all stressors draw from the same energy supply, the stressor effect, or the amount of energy used, is cumulative.

So, in order to determine the amount of stress we’re experiencing, we have to add up the energy used by all stressors we’re exposed to and weigh this against our energy supply. For example, the energy required for any physical activity would be added to the energy required for any mental activity, as well as the energy used for immune system function, breathing, digesting, and every other stressor we encounter.

While this may seem obvious, it actually poses a major problem for those in favor of hormesis.

Increasing exposure to hormetic factors is suggested as the answer for preventing or reversing degeneration, chronic disease, and obesity. And many common health recommendations, like caloric restriction, exercise, intermittent fasting, ketogenic and low-carb diets, and cold exposure, fall into this category of hormetic intervention.

But, in order for increasing exposure to hormetic factors to be the answer for preventing or reversing degeneration, chronic disease, and obesity, the people with these conditions would have to be experiencing too little stress!

And this is actually the argument that’s being made – it’s being suggested that because of our ample food supply, sedentarism, and general ease of life, we’re experiencing too little stress.

Now this obviously can’t be thought through too clearly if the same people who are suggesting that reading magazines or drinking ideal amounts of water are stressful enough to be hormetic are also suggesting that our 40+ hour workweeks, poor quality food, constant exposure to unnatural EMFs and chemical insults, and various other stressors are not stressful enough.

Along with all this is the lack of awareness that these factors, as well as a lack of sunlight, lack of sleep, lack of social interaction, and many other aspects of our modern lives, actually inhibit our ability to produce energy, so our capacity for handling increased energy demands is drastically reduced.

In fact, considering our capacity to handle stressors, we’re likely experiencing more stress now than we ever have before.

(Note: If you’re thinking that the presence of obesity means that we have excess energy and a lack of stress, take a look at these articles.)

All of this then has to make you wonder… if the dose-response follows a U-shaped curve, all of the stress and damage is cumulative, and every single factor in our environment causes us harm in order to maintain our health through protective adaptations, how could we ever have too little stress?

And if we instead go along with the assumption that we have too little stress despite the excessive number of stressors we consistently face, how could it ever be possible to be on the “too much stress” side of the curve?

As one researcher pointed out specifically in regard to chemical stressors:

… Calabrese maintains that maximal low-dose hormetic response (stimulation) occurs on average at a dose fivefold below the “no observed adverse effect level” (NOAEL). If this were the case, then simultaneous exposure to five or more compounds that are equally potent in eliciting a given response, each at a level one fifth of the NOAEL, would be enough to move an organism from the low-dose potentially “beneficial” range, to the range where adverse effects are expected. Given that residues of hundreds of chemicals can be measured in humans,31-35 many affecting the same tissues and fluctuating in concentration over the course of a lifetime, trying to titrate exposure to achieve a relatively narrow hormetic range is untenable.” (2)

And that’s only considering the toxic chemicals we’re exposed to, not the various “new” hormetic factors like water, exercise, and micronutrients.

Suffice it to say that when all these factors are accounted for, hormesis certainly fails as a scientific concept.

In fact, considering that adaptations to stress and damage don’t improve our health, stress and damage are cumulative, and that the benefits of environmental stimuli are due to their specific effects rather than the stress they cause, hormesis would be best characterized as an extreme misrepresentation of the interaction between the organism and its environment.

Preventing Stress

The idea that environmental factors are beneficial because of the stress or damage they cause is an incredibly dangerous premise, especially when it comes to regulating our exposure to toxic chemicals and radiation, and even more so when the cumulative effects of these exposures are considered.

As we’ve already acknowledged, stress is NOT beneficial and low doses of stress or damage do NOT result in adaptive benefits to the organism as a whole.   

Now, does this mean we should try to avoid anything that causes stress?

No, not at all.

In fact, we can’t!

All aspects of our environment can cause stress because they all demand energy. And we don’t need to avoid a stressor like exercise simply due to the stress it causes because its other beneficial effects can outweigh this stress.

So how do we determine which stressors we should avoid?

Selye described that our adaptation to a stimulus is dependent on the stimulus’s specific effects, stressor effects, and our internal environment. And, he explained that excessive amounts of stress lead to all sorts of symptoms and conditions.

This is because energy is the driver of our health and is needed for us to do anything and everything. So, the balance between the energy we produce and the energy we use is of utmost importance.

Any time our energy demands outweigh our energy supply, it encourages adaptations that allow us to make up for the energy deficit. While helpful in the short-term, these adaptations come at the cost of reducing our structural complexity and function, as these are both energy-dependent. They also result in adaptations that allow us to conserve energy to handle future stressors, which further reduce our structural complexity and function.

This energy deficiency and the resulting reduction in complexity and function underlies virtually all the negative health symptoms we may experience, from fatigue to a lack of libido to an inability to concentrate to constant hunger and cravings.

Excessive amounts of energy usage, or an excessive energy demand, is therefore extremely detrimental. And, optimizing energy production, or mitochondrial respiration, is the best way to increase our resistance and resilience to the stressors that we’ll inevitably experience.

So, exposing ourselves to factors with the least energy demand relative to their beneficial specific effects is ideal for our health. These specific effects would, on their deepest level, be measured by their ability to impact energy production.

In general, stressors that offer little benefit and are extremely energetically demanding or inhibiting, like ionizing radiation and endotoxin exposure, are best avoided, while other stressors that offer considerable benefit but can also be quite stressful, like exercise, are best used when they’re balanced with effective energy production.

If we were to evaluate the use of interventions like ketogenic diets, calorie restriction, or intermittent fasting through this lens, we’d see that they’re generally a terrible idea because they’re disastrous for energy production, which I’ve written about here.

As I mentioned earlier, there are potential benefits from these interventions that mostly stem from a lack of gut irritation, which would contribute towards improving energy production. But, these benefits can be attained in ways that don’t concurrently inhibit energy production, such as eating easily digestible foods and correcting gut function.

Along with these principles, it’s important to recognize our body’s natural drive for optimization and increased complexity. By providing it with adequate resources and minimal energy demands, it adapts by using increasing energy availability, allowing it to thrive and maximize its capabilities.

Dr. Ray Peat has effectively summated this idea in the following paragraph:

It’s important to minimize “low level” stressors and injuries, and to optimize the protective factors, such as light, carbohydrate, thyroid hormone, carbon dioxide, and a sense of a meaningful future. A positively beneficial environment supports constructive, and reconstructive, processes in the body that can correct much of the damage done by bad aspects of the environment, at any previous stage of development (Katz, et al., 1982; Yang, et al., 2015; Griñan-Ferré, et al., 2016; Kentner, et al., 2016). All of the body’s tissues, including the brain, are subject to revision and reconstruction. The weight of the brain, and the thickness of the cortex can be increased by environmental enrichment (Díaz, 1988; Rosenzweig and Bennett, 1996; Schrott, 1997; Lehohla, et al., 2004).” (121, emphasis mine)

In other words, in nearly complete opposition to the intentional exposure to stressful experiences encouraged by hormesis, minimizing stress relative to energy production is the KEY to regeneration and health.

So, I’ll conclude this oversized article with some of the most effective “anti-hormetic” things we can do to minimize stress and maximize energy production:

  • Eat a diet that’s composed of easily digestible foods, contains adequate nutrients (including sufficient calories and carbohydrates), and includes minimal amounts of toxins
  • Expose ourselves to a stimulating environment with rich social interaction
  • Stay active for the sake of enjoyment and movement rather than to expend as much energy as possible
  • Minimize our exposure to toxic and harmful chemicals and radiation
  • Minimize psychological stress

To dive deeper into these factors that drive energy production and minimize stress, be sure to sign up for the free health and energy balance mini-course below!

References

Hormesis Part 1: Does Stress Make You Stronger?

How many times have you heard that “what doesn’t kill you makes you stronger”?

This philosophy isn’t uncommon, and there is some truth to it, but it can also be incredibly dangerous.

Recently, an equivalent concept by the name of “hormesis” has been gaining traction in the alternative health sphere.

Hormesis is the idea that a small amount of stress or damage causes our body to adapt in a way that allows us to become stronger and improves our health.

You may be surprised to hear that many popular treatments, supplements, and dietary paradigms, like ketogenic diets, intermittent fasting, resveratrol, fish oil and omega-3s, and cold thermogenesis or cryotherapy, are grounded in this idea of hormesis (in these contexts it may also be referred to as mitohormesis). And the benefits of more classic interventions, like caloric restriction and exercise, are also now being attributed to hormesis.

It’s often said that these diets or treatments can improve mitochondrial function, increase cellular repair, promote autophagy, stimulate mitochondrial biogenesis, and cause other supposedly beneficial effects. These “hormetic effects” are all part of our adaptation to the stress caused by these interventions and are considered to be responsible for their health benefits.  

In other words, these interventions are known to cause stress, and it’s now being suggested that our adaptation to this stress is what makes these factors beneficial.

But, while hormesis sounds logical on the surface, as we dig deeper we’ll find that this concept is deeply flawed.

The Origins of Hormesis

Before we can determine whether the idea of hormesis is relevant to our physiology, we must first examine its origins and how it relates to stress and adaptation.

The idea of hormesis began with the suggestion that certain toxic agents (like ionizing radiation, methylmercury, and other poisons) triggered beneficial adaptive responses in low-doses. In other words, the minor damage they caused would improve our body’s natural defenses.

And, this idea happened to be a convenient justification for the negligence of various industries, as Dr. Ray Peat has summarized:

The idea that a little bit of something harmful is good for you was adopted by the petroleum, chemical and nuclear industries and their agents in government around 1950, and treated as a scientific concept, with the name ‘hormesis.’ When the public was starting to worry about the increased radioactivity of the environment because of nuclear bomb explosions, the US government was actively suppressing information on the increasing amount of environmental ionizing radiation, but they were even more active in promoting the idea that “small amounts” of radiation are harmless and even beneficial.” (1)

In addition to defending our exposure to small amounts of ionizing radiation, this idea has since been used to defend our exposure to low doses of pesticides, heavy metals like mercury and arsenic, toxic compounds in vaccines, chemotherapy drugs, endotoxin (also known as lipopolysaccharide or LPS), antinutrients and various polyphenols, and even cigarette smoke, among other things, by suggesting that not only are small amounts of these toxic factors not harmful, they’re actually beneficial due to the adaptive responses they cause (2, 3, 4, 5, 6, 7, 8).

According to this original definition of hormesis, the response to these toxic factors followed the curve shown below in Figure 1.


Fig 1. Image taken from this study

This curve represents the idea that at very small doses, these factors would create a beneficial response (the maximum response). Then at a certain dose, the NOAEL (meaning the no observed adverse effect level) would be reached, where the toxic factor supposedly has no net effect on the organism. Then, at any dose after the NOAEL, the toxic exposure would be harmful.

It’s important to note that the average dose used for the supposed hormetic effect (at the “maximum response”) is 5 times lower than the dose at the NOAEL (where there is no net effect on the organism), so we’re talking about extremely small doses of these toxic factors.

There are several issues with this original notion that I’ll touch on throughout this article, but one of the most important to note is that the “benefits” seen at these very low doses of toxic factors come at the cost of harm elsewhere (2, 3, 9).

Hormetic doses of dioxin (TCDD), for example, were shown to reduce cancer incidence in the pituitary, uterus, mammary glands, pancreas, and adrenal glands. But, the same dose increased cancer incidence in the liver, lung, tongue, and nasal turbinates (9). And hormetic doses of cadmium have been shown to cause non-statistically significant reductions in testicular tumors but also an increase in the incidence of prostate tumors (9).

These flaws aside, the concept of hormesis has undergone quite an expansion in recent decades that’s made its definition quite difficult to nail down.

Instead of referring only to the supposedly beneficial adaptations that result from the damage caused by very low doses of toxic environmental agents, the concept is now being applied to any factor that exhibits a biphasic (or triphasic) dose-response rather than a linear dose-response.

This includes any stimulus that follows normal or inverted J-shaped dose-response curves (like in Figure 1) or U-shaped curves, like the one depicted here:


Fig 2. Image taken from this study

In relation to hormesis, the J-shaped curve characterizes the idea that lower doses of a substance are beneficial while higher doses are harmful. And the U-shaped curve characterizes the idea that moderate amounts of a substance are beneficial, but too little or too much is harmful.

(Note: the effects can also be reversed if the curves are inverted.)

The conflation of these two mostly independent phenomena (the adaptive response to toxins and the biphasic or triphasic dose-response) has resulted in a 2nd definition of hormesis that’s no longer restricted to exposure to very low doses of toxins, and can instead be applied to virtually all environmental inputs.

This is because factors that follow these response curves are extremely common, including everything from exercise to sunlight exposure to vitamins and minerals. And, in accordance with the original definition of hormesis, researchers are attributing the effects of the factors following these dose-response curves to defensive adaptations in response to stress.

So, they’re suggesting that the benefits from exercise, ketogenic diets, caloric restriction, sunlight, cold or heat exposure, and even from essential nutrients like water, vitamins, and minerals, are due to the stress, or “hormetic effects,” they supposedly cause (4, 6, 7, 8, 10, 11, 12, 13).

And considering the original concept of hormesis, this isn’t such a stretch.

Those in favor of this idea suggest that the stress caused by these factors causes the body to adapt in a way that protects it from future stress. This then supposedly results in beneficial effects like DNA repair, antioxidant production, autophagy (the recycling of cellular components), increased lifespan, increased mitochondrial function, increased resistance to stress, and overall improved health.

To muddy the waters even further, other researchers are operating on a 3rd definition of hormesis, where they entirely ignore the stress component and determine hormetic factors solely based on the non-linear dose-response curves (13).

In this series of articles, I’ll be focusing on the 2nd of these 3 definitions, where the health benefits of all factors that follow these non-linear dose-response curves are attributed to the adaptive response to the stress they cause. This is the definition that’s most relevant and most commonly used to defend the use of various health-related hormetic interventions.

To summarize this definition succinctly, you could simply say that it’s the idea that small amounts of stress are beneficial to our health because they improve our body’s defenses, and that this stress is responsible for the health benefits of virtually all aspects of our environment.

(Note: The latter part of this definition isn’t agreed upon by all in favor of hormesis.)

Now in order to understand the flaws with this concept, we must explore the relationship between stress and adaptation.

Stress and Adaptation

Hans Selye’s work was pivotal in forming our understanding of stress and adaptation.

Selye recognized that all stimuli have unique, specific effects on our physiology. Exercise, for example, causes tension on our musculofascial system, while sunlight exposure causes vitamin D to be produced from cholesterol (among other things). But, Selye was the first to elucidate the idea that all stimuli also share a common or generalized effect.

This common or generalized effect occurs on the bioenergetic level. All stimuli increase the usage of energy to some degree, which is called the stressor effect. Additionally, stimuli can either encourage or inhibit the production of energy, which we’ll be diving into later on in this series.

(Note: By “energy” I’m referring to physiological energy produced from mitochondrial respiration, which I describe further in this article.)

Hans Selye also described our body’s response to stimuli, or adaptation. Our bodies are constantly adapting, to every stimulus they’re faced with, in order to best adjust to their environment. This adaptation is dependent on both the stimulus’s specific effects and energetic effects, as well as on our internal environment.

Let’s consider how we adapt to stimuli based on each of these effects.

Our adaptations to specific effects are unique to each stimulus.

If we’re exposed to sunlight, our skin darkens by increasing melanin production so we don’t burn as easily. If we exercise, the muscles we use will grow and our neuromuscular connections will strengthen, allowing our muscles to produce greater amounts of force. And if we’re exposed to high ambient temperatures, our blood volume increases so we can sweat more and cool ourselves easier.

Our adaptations to the bioenergetic effects of stimuli, on the other hand, are directly related to our energy balance, or the balance between our energy supply and energy demand.

Energy drives our health and is needed for us to do anything and everything. When we have an energy deficit, our body reacts with a generalized response called the stress response (or just “stress”), which is primarily characterized by the release of stress hormones. These stress hormones allow for energy to be produced to make up for the energy deficit, which allows us to continue to function.

(Note: It’s important to point out that this stress isn’t the same as “psychological stress,” which is an emotional response. However, this emotional response can actually be both caused by stress and a cause of stress, as I explained here.)

So, the increased usage of energy or the inhibition of energy production by any stimulus can cause an energy deficit, leading to stress.

Over time, in response to this energy deficit, our body adapts by reducing the energy it uses and produces in order to conserve fuel and promote survival, which better prepares us to handle future stress at the cost of slowing our high-level functions. This adaptation is driven by increases in stress hormones over time, which I detailed in this article.

If we instead have an energy surplus, we adapt by increasing the amount of energy we use, which improves the functioning of our brain, digestive system, immune system, and other high-level functions. Our body will also favor energy production in place of fuel conservation, which allows us to further improve these functions and increases the pool of energy that we can draw from when we experience minor stressors, which then reduces harmful adaptations.

In this way, you could consider these adaptations to be positive feedback loops, where greater energy availability further increases energy availability and reduced energy availability further reduces energy availability.

Because of these adaptive mechanisms, our body will always adapt to stress in a way that encourages the conservation of fuel and energy and subsequently reduces higher-level functions. However, we must also keep in mind that the amount of energy we have available to deal with the stressors will determine the extent of these adaptations.

So, when analyzing the effects of any stimulus, we must weigh the beneficial and harmful specific effects of the stimulus with its stress-promoting or stress-inhibiting bioenergetic effects.

We must also consider that, because energetic effects are common between all stimuli, the effects are cumulative. So, in order to determine the total stress on an organism, we must consider the bioenergetic inputs from all factors in its environment.

Hormesis and Adaptation

How does all this tie into hormesis?

Well, hormesis began by suggesting that the specific effects of certain toxic agents (like ionizing radiation, methylmercury, and other poisons) caused beneficial adaptive responses. In other words, the damage they caused improved our defenses.

Then, hormesis morphed into the idea that the stress-promoting effects of all factors (like fasting, exercise, vitamins, and water) cause beneficial adaptive responses.

Underlying both definitions is the idea that the adaptive defensive reactions caused by stress or damage improve our health and allow us to function optimally. But, while this may sound logical on the surface, it’s really a reductionistic mischaracterization of adaptation.

Part of this mischaracterization is due to a lack of understanding of bioenergetics and an assumption that excess energy is actually harmful. This isn’t uncommon thinking nowadays, as obesity is blamed on “overnutrition” or “excess energy,” even though it’s a condition characterized by a lack of energy, like all chronic diseases. (You can find out more about the relationship between fat loss and energy in these articles.)

As you read earlier in relation to adaptation, excess energy allows us to adapt to our environment in a way that improves our overall function. And on the opposite end of the spectrum, when we’re exposed to a stressful or energy-demanding environment, we adapt in the opposite way to best fit that environment.

That means that, rather than expending our energy on having a high-functioning, high-performance system, we use our energy to deal with the stressful environment that we’re faced with and conserve our fuel to prepare for future stress.

As Dr. Ray Peat has explained, “if the environments that the organism encounters are abundant in resources the organism will develop its capacity, tending to maximize its ability to interact constructively.” However, “defensive reactions that simply assure survival often degrade functioning of the individual” (1).

So, the entire adaptive model from which hormesis operates is flawed – adaptations to stress do improve our ability to handle stress, but this comes at the cost of degrading our overall functional capacity.

In this article we’ve set the stage for the 2nd part of this series, where we’ll dig into the research supporting hormesis and identify its major flaws. We’ll also take a look at the many misapplications that have resulted from this flawed research, including ketogenic diets, intermittent fasting, caloric restriction, and more. Lastly, we’ll explore why stress is inherently harmful, but why we may not want to avoid everything that causes stress.

References

Hormesis Part 1: Does Stress Make You Stronger?

How many times have you heard that “what doesn’t kill you makes you stronger”?

This philosophy isn’t uncommon, and there is some truth to it, but it can also be incredibly dangerous.

Recently, an equivalent concept by the name of “hormesis” has been gaining traction in the alternative health sphere.

Hormesis is the idea that a small amount of stress or damage causes our body to adapt in a way that allows us to become stronger and improves our health.

You may be surprised to hear that many popular treatments, supplements, and dietary paradigms, like ketogenic diets, intermittent fasting, resveratrol, fish oil and omega-3s, and cold thermogenesis or cryotherapy, are grounded in this idea of hormesis (in these contexts it may also be referred to as mitohormesis). And the benefits of more classic interventions, like caloric restriction and exercise, are also now being attributed to hormesis.

It’s often said that these diets or treatments can improve mitochondrial function, increase cellular repair, promote autophagy, stimulate mitochondrial biogenesis, and cause other supposedly beneficial effects. These “hormetic effects” are all part of our adaptation to the stress caused by these interventions and are considered to be responsible for their health benefits.  

In other words, these interventions are known to cause stress, and it’s now being suggested that our adaptation to this stress is what makes these factors beneficial.

But, while hormesis sounds logical on the surface, as we dig deeper we’ll find that this concept is deeply flawed.

The Origins of Hormesis

Before we can determine whether the idea of hormesis is relevant to our physiology, we must first examine its origins and how it relates to stress and adaptation.

The idea of hormesis began with the suggestion that certain toxic agents (like ionizing radiation, methylmercury, and other poisons) triggered beneficial adaptive responses in low-doses. In other words, the minor damage they caused would improve our body’s natural defenses.

And, this idea happened to be a convenient justification for the negligence of various industries, as Dr. Ray Peat has summarized:

The idea that a little bit of something harmful is good for you was adopted by the petroleum, chemical and nuclear industries and their agents in government around 1950, and treated as a scientific concept, with the name ‘hormesis.’ When the public was starting to worry about the increased radioactivity of the environment because of nuclear bomb explosions, the US government was actively suppressing information on the increasing amount of environmental ionizing radiation, but they were even more active in promoting the idea that “small amounts” of radiation are harmless and even beneficial.” (1)

In addition to defending our exposure to small amounts of ionizing radiation, this idea has since been used to defend our exposure to low doses of pesticides, heavy metals like mercury and arsenic, toxic compounds in vaccines, chemotherapy drugs, endotoxin (also known as lipopolysaccharide or LPS), antinutrients and various polyphenols, and even cigarette smoke, among other things, by suggesting that not only are small amounts of these toxic factors not harmful, they’re actually beneficial due to the adaptive responses they cause (2, 3, 4, 5, 6, 7, 8).

According to this original definition of hormesis, the response to these toxic factors followed the curve shown below in Figure 1.


Fig 1. Image taken from this study

This curve represents the idea that at very small doses, these factors would create a beneficial response (the maximum response). Then at a certain dose, the NOAEL (meaning the no observed adverse effect level) would be reached, where the toxic factor supposedly has no net effect on the organism. Then, at any dose after the NOAEL, the toxic exposure would be harmful.

It’s important to note that the average dose used for the supposed hormetic effect (at the “maximum response”) is 5 times lower than the dose at the NOAEL (where there is no net effect on the organism), so we’re talking about extremely small doses of these toxic factors.

There are several issues with this original notion that I’ll touch on throughout this article, but one of the most important to note is that the “benefits” seen at these very low doses of toxic factors come at the cost of harm elsewhere (2, 3, 9).

Hormetic doses of dioxin (TCDD), for example, were shown to reduce cancer incidence in the pituitary, uterus, mammary glands, pancreas, and adrenal glands. But, the same dose increased cancer incidence in the liver, lung, tongue, and nasal turbinates (9). And hormetic doses of cadmium have been shown to cause non-statistically significant reductions in testicular tumors but also an increase in the incidence of prostate tumors (9).

These flaws aside, the concept of hormesis has undergone quite an expansion in recent decades that’s made its definition quite difficult to nail down.

Instead of referring only to the supposedly beneficial adaptations that result from the damage caused by very low doses of toxic environmental agents, the concept is now being applied to any factor that exhibits a biphasic (or triphasic) dose-response rather than a linear dose-response.

This includes any stimulus that follows normal or inverted J-shaped dose-response curves (like in Figure 1) or U-shaped curves, like the one depicted here:


Fig 2. Image taken from this study

In relation to hormesis, the J-shaped curve characterizes the idea that lower doses of a substance are beneficial while higher doses are harmful. And the U-shaped curve characterizes the idea that moderate amounts of a substance are beneficial, but too little or too much is harmful.

(Note: the effects can also be reversed if the curves are inverted.)

The conflation of these two mostly independent phenomena (the adaptive response to toxins and the biphasic or triphasic dose-response) has resulted in a 2nd definition of hormesis that’s no longer restricted to exposure to very low doses of toxins, and can instead be applied to virtually all environmental inputs.

This is because factors that follow these response curves are extremely common, including everything from exercise to sunlight exposure to vitamins and minerals. And, in accordance with the original definition of hormesis, researchers are attributing the effects of the factors following these dose-response curves to defensive adaptations in response to stress.

So, they’re suggesting that the benefits from exercise, ketogenic diets, caloric restriction, sunlight, cold or heat exposure, and even from essential nutrients like water, vitamins, and minerals, are due to the stress, or “hormetic effects,” they supposedly cause (4, 6, 7, 8, 10, 11, 12, 13).

And considering the original concept of hormesis, this isn’t such a stretch.

Those in favor of this idea suggest that the stress caused by these factors causes the body to adapt in a way that protects it from future stress. This then supposedly results in beneficial effects like DNA repair, antioxidant production, autophagy (the recycling of cellular components), increased lifespan, increased mitochondrial function, increased resistance to stress, and overall improved health.

To muddy the waters even further, other researchers are operating on a 3rd definition of hormesis, where they entirely ignore the stress component and determine hormetic factors solely based on the non-linear dose-response curves (13).

In this series of articles, I’ll be focusing on the 2nd of these 3 definitions, where the health benefits of all factors that follow these non-linear dose-response curves are attributed to the adaptive response to the stress they cause. This is the definition that’s most relevant and most commonly used to defend the use of various health-related hormetic interventions.

To summarize this definition succinctly, you could simply say that it’s the idea that small amounts of stress are beneficial to our health because they improve our body’s defenses, and that this stress is responsible for the health benefits of virtually all aspects of our environment.

(Note: The latter part of this definition isn’t agreed upon by all in favor of hormesis.)

Now in order to understand the flaws with this concept, we must explore the relationship between stress and adaptation.

Stress and Adaptation

Hans Selye’s work was pivotal in forming our understanding of stress and adaptation.

Selye recognized that all stimuli have unique, specific effects on our physiology. Exercise, for example, causes tension on our musculofascial system, while sunlight exposure causes vitamin D to be produced from cholesterol (among other things). But, Selye was the first to elucidate the idea that all stimuli also share a common or generalized effect.

This common or generalized effect occurs on the bioenergetic level. All stimuli increase the usage of energy to some degree, which is called the stressor effect. Additionally, stimuli can either encourage or inhibit the production of energy, which we’ll be diving into later on in this series.

(Note: By “energy” I’m referring to physiological energy produced from mitochondrial respiration, which I describe further in this article.)

Hans Selye also described our body’s response to stimuli, or adaptation. Our bodies are constantly adapting, to every stimulus they’re faced with, in order to best adjust to their environment. This adaptation is dependent on both the stimulus’s specific effects and energetic effects, as well as on our internal environment.

Let’s consider how we adapt to stimuli based on each of these effects.

Our adaptations to specific effects are unique to each stimulus.

If we’re exposed to sunlight, our skin darkens by increasing melanin production so we don’t burn as easily. If we exercise, the muscles we use will grow and our neuromuscular connections will strengthen, allowing our muscles to produce greater amounts of force. And if we’re exposed to high ambient temperatures, our blood volume increases so we can sweat more and cool ourselves easier.

Our adaptations to the bioenergetic effects of stimuli, on the other hand, are directly related to our energy balance, or the balance between our energy supply and energy demand.

Energy drives our health and is needed for us to do anything and everything. When we have an energy deficit, our body reacts with a generalized response called the stress response (or just “stress”), which is primarily characterized by the release of stress hormones. These stress hormones allow for energy to be produced to make up for the energy deficit, which allows us to continue to function.

(Note: It’s important to point out that this stress isn’t the same as “psychological stress,” which is an emotional response. However, this emotional response can actually be both caused by stress and a cause of stress, as I explained here.)

So, the increased usage of energy or the inhibition of energy production by any stimulus can cause an energy deficit, leading to stress.

Over time, in response to this energy deficit, our body adapts by reducing the energy it uses and produces in order to conserve fuel and promote survival, which better prepares us to handle future stress at the cost of slowing our high-level functions. This adaptation is driven by increases in stress hormones over time, which I detailed in this article.

If we instead have an energy surplus, we adapt by increasing the amount of energy we use, which improves the functioning of our brain, digestive system, immune system, and other high-level functions. Our body will also favor energy production in place of fuel conservation, which allows us to further improve these functions and increases the pool of energy that we can draw from when we experience minor stressors, which then reduces harmful adaptations.

In this way, you could consider these adaptations to be positive feedback loops, where greater energy availability further increases energy availability and reduced energy availability further reduces energy availability.

Because of these adaptive mechanisms, our body will always adapt to stress in a way that encourages the conservation of fuel and energy and subsequently reduces higher-level functions. However, we must also keep in mind that the amount of energy we have available to deal with the stressors will determine the extent of these adaptations.

So, when analyzing the effects of any stimulus, we must weigh the beneficial and harmful specific effects of the stimulus with its stress-promoting or stress-inhibiting bioenergetic effects.

We must also consider that, because energetic effects are common between all stimuli, the effects are cumulative. So, in order to determine the total stress on an organism, we must consider the bioenergetic inputs from all factors in its environment.

Hormesis and Adaptation

How does all this tie into hormesis?

Well, hormesis began by suggesting that the specific effects of certain toxic agents (like ionizing radiation, methylmercury, and other poisons) caused beneficial adaptive responses. In other words, the damage they caused improved our defenses.

Then, hormesis morphed into the idea that the stress-promoting effects of all factors (like fasting, exercise, vitamins, and water) cause beneficial adaptive responses.

Underlying both definitions is the idea that the adaptive defensive reactions caused by stress or damage improve our health and allow us to function optimally. But, while this may sound logical on the surface, it’s really a reductionistic mischaracterization of adaptation.

Part of this mischaracterization is due to a lack of understanding of bioenergetics and an assumption that excess energy is actually harmful. This isn’t uncommon thinking nowadays, as obesity is blamed on “overnutrition” or “excess energy,” even though it’s a condition characterized by a lack of energy, like all chronic diseases. (You can find out more about the relationship between fat loss and energy in these articles.)

As you read earlier in relation to adaptation, excess energy allows us to adapt to our environment in a way that improves our overall function. And on the opposite end of the spectrum, when we’re exposed to a stressful or energy-demanding environment, we adapt in the opposite way to best fit that environment.

That means that, rather than expending our energy on having a high-functioning, high-performance system, we use our energy to deal with the stressful environment that we’re faced with and conserve our fuel to prepare for future stress.

As Dr. Ray Peat has explained, “if the environments that the organism encounters are abundant in resources the organism will develop its capacity, tending to maximize its ability to interact constructively.” However, “defensive reactions that simply assure survival often degrade functioning of the individual” (1).

So, the entire adaptive model from which hormesis operates is flawed – adaptations to stress do improve our ability to handle stress, but this comes at the cost of degrading our overall functional capacity.

In this article we’ve set the stage for the 2nd part of this series, where we’ll dig into the research supporting hormesis and identify its major flaws. We’ll also take a look at the many misapplications that have resulted from this flawed research, including ketogenic diets, intermittent fasting, caloric restriction, and more. Lastly, we’ll explore why stress is inherently harmful, but why we may not want to avoid everything that causes stress.

References

Hormesis Part 1: Does Stress Make You Stronger?

How many times have you heard that “what doesn’t kill you makes you stronger”?

This philosophy isn’t uncommon, and there is some truth to it, but it can also be incredibly dangerous.

Recently, an equivalent concept by the name of “hormesis” has been gaining traction in the alternative health sphere.

Hormesis is the idea that a small amount of stress or damage causes our body to adapt in a way that allows us to become stronger and improves our health.

You may be surprised to hear that many popular treatments, supplements, and dietary paradigms, like ketogenic diets, intermittent fasting, resveratrol, fish oil and omega-3s, and cold thermogenesis or cryotherapy, are grounded in this idea of hormesis (in these contexts it may also be referred to as mitohormesis). And the benefits of more classic interventions, like caloric restriction and exercise, are also now being attributed to hormesis.

It’s often said that these diets or treatments can improve mitochondrial function, increase cellular repair, promote autophagy, stimulate mitochondrial biogenesis, and cause other supposedly beneficial effects. These “hormetic effects” are all part of our adaptation to the stress caused by these interventions and are considered to be responsible for their health benefits.  

In other words, these interventions are known to cause stress, and it’s now being suggested that our adaptation to this stress is what makes these factors beneficial.

But, while hormesis sounds logical on the surface, as we dig deeper we’ll find that this concept is deeply flawed.

The Origins of Hormesis

Before we can determine whether the idea of hormesis is relevant to our physiology, we must first examine its origins and how it relates to stress and adaptation.

The idea of hormesis began with the suggestion that certain toxic agents (like ionizing radiation, methylmercury, and other poisons) triggered beneficial adaptive responses in low-doses. In other words, the minor damage they caused would improve our body’s natural defenses.

And, this idea happened to be a convenient justification for the negligence of various industries, as Dr. Ray Peat has summarized:

The idea that a little bit of something harmful is good for you was adopted by the petroleum, chemical and nuclear industries and their agents in government around 1950, and treated as a scientific concept, with the name ‘hormesis.’ When the public was starting to worry about the increased radioactivity of the environment because of nuclear bomb explosions, the US government was actively suppressing information on the increasing amount of environmental ionizing radiation, but they were even more active in promoting the idea that “small amounts” of radiation are harmless and even beneficial.” (1)

In addition to defending our exposure to small amounts of ionizing radiation, this idea has since been used to defend our exposure to low doses of pesticides, heavy metals like mercury and arsenic, toxic compounds in vaccines, chemotherapy drugs, endotoxin (also known as lipopolysaccharide or LPS), antinutrients and various polyphenols, and even cigarette smoke, among other things, by suggesting that not only are small amounts of these toxic factors not harmful, they’re actually beneficial due to the adaptive responses they cause (2, 3, 4, 5, 6, 7, 8).

According to this original definition of hormesis, the response to these toxic factors followed the curve shown below in Figure 1.


Fig 1. Image taken from this study

This curve represents the idea that at very small doses, these factors would create a beneficial response (the maximum response). Then at a certain dose, the NOAEL (meaning the no observed adverse effect level) would be reached, where the toxic factor supposedly has no net effect on the organism. Then, at any dose after the NOAEL, the toxic exposure would be harmful.

It’s important to note that the average dose used for the supposed hormetic effect (at the “maximum response”) is 5 times lower than the dose at the NOAEL (where there is no net effect on the organism), so we’re talking about extremely small doses of these toxic factors.

There are several issues with this original notion that I’ll touch on throughout this article, but one of the most important to note is that the “benefits” seen at these very low doses of toxic factors come at the cost of harm elsewhere (2, 3, 9).

Hormetic doses of dioxin (TCDD), for example, were shown to reduce cancer incidence in the pituitary, uterus, mammary glands, pancreas, and adrenal glands. But, the same dose increased cancer incidence in the liver, lung, tongue, and nasal turbinates (9). And hormetic doses of cadmium have been shown to cause non-statistically significant reductions in testicular tumors but also an increase in the incidence of prostate tumors (9).

These flaws aside, the concept of hormesis has undergone quite an expansion in recent decades that’s made its definition quite difficult to nail down.

Instead of referring only to the supposedly beneficial adaptations that result from the damage caused by very low doses of toxic environmental agents, the concept is now being applied to any factor that exhibits a biphasic (or triphasic) dose-response rather than a linear dose-response.

This includes any stimulus that follows normal or inverted J-shaped dose-response curves (like in Figure 1) or U-shaped curves, like the one depicted here:


Fig 2. Image taken from this study

In relation to hormesis, the J-shaped curve characterizes the idea that lower doses of a substance are beneficial while higher doses are harmful. And the U-shaped curve characterizes the idea that moderate amounts of a substance are beneficial, but too little or too much is harmful.

(Note: the effects can also be reversed if the curves are inverted.)

The conflation of these two mostly independent phenomena (the adaptive response to toxins and the biphasic or triphasic dose-response) has resulted in a 2nd definition of hormesis that’s no longer restricted to exposure to very low doses of toxins, and can instead be applied to virtually all environmental inputs.

This is because factors that follow these response curves are extremely common, including everything from exercise to sunlight exposure to vitamins and minerals. And, in accordance with the original definition of hormesis, researchers are attributing the effects of the factors following these dose-response curves to defensive adaptations in response to stress.

So, they’re suggesting that the benefits from exercise, ketogenic diets, caloric restriction, sunlight, cold or heat exposure, and even from essential nutrients like water, vitamins, and minerals, are due to the stress, or “hormetic effects,” they supposedly cause (4, 6, 7, 8, 10, 11, 12, 13).

And considering the original concept of hormesis, this isn’t such a stretch.

Those in favor of this idea suggest that the stress caused by these factors causes the body to adapt in a way that protects it from future stress. This then supposedly results in beneficial effects like DNA repair, antioxidant production, autophagy (the recycling of cellular components), increased lifespan, increased mitochondrial function, increased resistance to stress, and overall improved health.

To muddy the waters even further, other researchers are operating on a 3rd definition of hormesis, where they entirely ignore the stress component and determine hormetic factors solely based on the non-linear dose-response curves (13).

In this series of articles, I’ll be focusing on the 2nd of these 3 definitions, where the health benefits of all factors that follow these non-linear dose-response curves are attributed to the adaptive response to the stress they cause. This is the definition that’s most relevant and most commonly used to defend the use of various health-related hormetic interventions.

To summarize this definition succinctly, you could simply say that it’s the idea that small amounts of stress are beneficial to our health because they improve our body’s defenses, and that this stress is responsible for the health benefits of virtually all aspects of our environment.

(Note: The latter part of this definition isn’t agreed upon by all in favor of hormesis.)

Now in order to understand the flaws with this concept, we must explore the relationship between stress and adaptation.

Stress and Adaptation

Hans Selye’s work was pivotal in forming our understanding of stress and adaptation.

Selye recognized that all stimuli have unique, specific effects on our physiology. Exercise, for example, causes tension on our musculofascial system, while sunlight exposure causes vitamin D to be produced from cholesterol (among other things). But, Selye was the first to elucidate the idea that all stimuli also share a common or generalized effect.

This common or generalized effect occurs on the bioenergetic level. All stimuli increase the usage of energy to some degree, which is called the stressor effect. Additionally, stimuli can either encourage or inhibit the production of energy, which we’ll be diving into later on in this series.

(Note: By “energy” I’m referring to physiological energy produced from mitochondrial respiration, which I describe further in this article.)

Hans Selye also described our body’s response to stimuli, or adaptation. Our bodies are constantly adapting, to every stimulus they’re faced with, in order to best adjust to their environment. This adaptation is dependent on both the stimulus’s specific effects and energetic effects, as well as on our internal environment.

Let’s consider how we adapt to stimuli based on each of these effects.

Our adaptations to specific effects are unique to each stimulus.

If we’re exposed to sunlight, our skin darkens by increasing melanin production so we don’t burn as easily. If we exercise, the muscles we use will grow and our neuromuscular connections will strengthen, allowing our muscles to produce greater amounts of force. And if we’re exposed to high ambient temperatures, our blood volume increases so we can sweat more and cool ourselves easier.

Our adaptations to the bioenergetic effects of stimuli, on the other hand, are directly related to our energy balance, or the balance between our energy supply and energy demand.

Energy drives our health and is needed for us to do anything and everything. When we have an energy deficit, our body reacts with a generalized response called the stress response (or just “stress”), which is primarily characterized by the release of stress hormones. These stress hormones allow for energy to be produced to make up for the energy deficit, which allows us to continue to function.

(Note: It’s important to point out that this stress isn’t the same as “psychological stress,” which is an emotional response. However, this emotional response can actually be both caused by stress and a cause of stress, as I explained here.)

So, the increased usage of energy or the inhibition of energy production by any stimulus can cause an energy deficit, leading to stress.

Over time, in response to this energy deficit, our body adapts by reducing the energy it uses and produces in order to conserve fuel and promote survival, which better prepares us to handle future stress at the cost of slowing our high-level functions. This adaptation is driven by increases in stress hormones over time, which I detailed in this article.

If we instead have an energy surplus, we adapt by increasing the amount of energy we use, which improves the functioning of our brain, digestive system, immune system, and other high-level functions. Our body will also favor energy production in place of fuel conservation, which allows us to further improve these functions and increases the pool of energy that we can draw from when we experience minor stressors, which then reduces harmful adaptations.

In this way, you could consider these adaptations to be positive feedback loops, where greater energy availability further increases energy availability and reduced energy availability further reduces energy availability.

Because of these adaptive mechanisms, our body will always adapt to stress in a way that encourages the conservation of fuel and energy and subsequently reduces higher-level functions. However, we must also keep in mind that the amount of energy we have available to deal with the stressors will determine the extent of these adaptations.

So, when analyzing the effects of any stimulus, we must weigh the beneficial and harmful specific effects of the stimulus with its stress-promoting or stress-inhibiting bioenergetic effects.

We must also consider that, because energetic effects are common between all stimuli, the effects are cumulative. So, in order to determine the total stress on an organism, we must consider the bioenergetic inputs from all factors in its environment.

Hormesis and Adaptation

How does all this tie into hormesis?

Well, hormesis began by suggesting that the specific effects of certain toxic agents (like ionizing radiation, methylmercury, and other poisons) caused beneficial adaptive responses. In other words, the damage they caused improved our defenses.

Then, hormesis morphed into the idea that the stress-promoting effects of all factors (like fasting, exercise, vitamins, and water) cause beneficial adaptive responses.

Underlying both definitions is the idea that the adaptive defensive reactions caused by stress or damage improve our health and allow us to function optimally. But, while this may sound logical on the surface, it’s really a reductionistic mischaracterization of adaptation.

Part of this mischaracterization is due to a lack of understanding of bioenergetics and an assumption that excess energy is actually harmful. This isn’t uncommon thinking nowadays, as obesity is blamed on “overnutrition” or “excess energy,” even though it’s a condition characterized by a lack of energy, like all chronic diseases. (You can find out more about the relationship between fat loss and energy in these articles.)

As you read earlier in relation to adaptation, excess energy allows us to adapt to our environment in a way that improves our overall function. And on the opposite end of the spectrum, when we’re exposed to a stressful or energy-demanding environment, we adapt in the opposite way to best fit that environment.

That means that, rather than expending our energy on having a high-functioning, high-performance system, we use our energy to deal with the stressful environment that we’re faced with and conserve our fuel to prepare for future stress.

As Dr. Ray Peat has explained, “if the environments that the organism encounters are abundant in resources the organism will develop its capacity, tending to maximize its ability to interact constructively.” However, “defensive reactions that simply assure survival often degrade functioning of the individual” (1).

So, the entire adaptive model from which hormesis operates is flawed – adaptations to stress do improve our ability to handle stress, but this comes at the cost of degrading our overall functional capacity.

In this article we’ve set the stage for the 2nd part of this series, where we’ll dig into the research supporting hormesis and identify its major flaws. We’ll also take a look at the many misapplications that have resulted from this flawed research, including ketogenic diets, intermittent fasting, caloric restriction, and more. Lastly, we’ll explore why stress is inherently harmful, but why we may not want to avoid everything that causes stress.

References

Is Depression Really Caused By A Chemical Imbalance?

I know this is a touchy subject.

Not only is mental health a very personal issue, but there’s a stigma surrounding mental health disorders that often comes in the form of blaming those who have these issues or even discounting the legitimacy of these disorders.

And, those who aren’t in favor of the chemical imbalance theory often get lumped in with the people who stigmatize these disorders. Because of these associations, I want to first clarify that I’m NOT blaming anyone for their state of mental health nor am I discounting that these conditions are legitimate and biological in nature.

With that out of the way, we can talk about what’s really causing mental health disorders like depression.

The mainstream belief is that these conditions are caused by specific chemical imbalances in the brain and that these imbalances can only be fixed with prescription medications. This is also known as the “chemical imbalance theory.”

This theory has, in part, led to a dramatic rise in the prescription of antidepressant medications over the past few decades, to the point that over 10% of Americans are taking antidepressants. It has also fueled the massive growth of the multi-billion-dollar antidepressant drug industry.

But, this mainstream theory doesn’t hold up and these medications are not the solution to the growing problem of depression and other mental health disorders.

The Many Flaws of The Chemical Imbalance Theory

First, I’d like to make it clear that I’m not suggesting that the chemicals in our brains don’t affect our mental health. In fact, I would go as far as to say the exact opposite: our mental health and physical health are inextricably linked to the point that there really is no separation – our mental health isn’t at all distinct from our physiology.

And this leads us to one of the biggest flaws of the chemical imbalance theory, which is that the hormones and neurotransmitters that affect our mental health aren’t affected by what’s going on in the rest of our body.

The idea that our mind is separate from our body is extremely common. It’s assumed that our thoughts, mood, and outlook on life are completely independent of the foods we eat, chemicals we’re exposed to, sunlight we get, and all other factors of our environment. But this isn’t at all the case.

There’s no true separation between our mind and body. All these environmental factors affect us on a physiological level, and this includes affecting the many aspects of brain physiology that are related to our thoughts, mood, and perspective through which we see the world. This includes effects on our “brain chemicals,” like serotonin, dopamine, GABA, and norepinephrine.

So the issue isn’t determining whether chemicals in our brain affect our thoughts or mood, the issue is the thinking that these chemicals can’t be changed by our environment and instead are, presumably, primarily genetically determined. This then suggests that there’s nothing we can do about these “chemical imbalances” other than fixing them with prescription medications.

Along with this misconception is the fallacy that mental health disorders as complex as depression can be broken down to simple chemical imbalances (too little or too much of a single neurotransmitter, for example), which is what the antidepressant medications are aimed at treating.

Perhaps surprisingly, these flaws have been extensively acknowledged in the scientific literature:

While neuroscience is a rapidly advancing field, to propose that researchers can objectively identify a “chemical imbalance” at the molecular level is not compatible with the extant science. In fact, there is no scientifically established ideal “chemical balance” of serotonin, let alone an identifiable pathological imbalance. To equate the impressive recent achievements of neuroscience with support for the serotonin hypothesis is a mistake.” (1)

In short, there exists no rigorous corroboration of the serotonin theory, and a significant body of contradictory evidence. Far from being a radical line of thought, doubts about the serotonin hypothesis are well acknowledged by many researchers, including frank statements from prominent psychiatrists, some of whom are even enthusiastic proponents of SSRI medications.” (1)

Nonetheless, the chemical imbalance theory is still the popular narrative outside of the scientific literature. While this theory is heavily flawed, it wouldn’t be nearly as dangerous if the prescribed medications were actually safe and effective.

Antidepressants are some of the most prescribed drugs in the United States, the most common of which are SSRIs. These medications are based on the idea that depression is caused by a lack of serotonin, a notion that has become so pervasive that serotonin is colloquially considered the “happy hormone.” Simply put, this is absolutely not the case, but I’ll dig into that in more detail another time. For now, the complete failure of these drugs will have to do as evidence against this supposition.

Antidepressant drugs are incredibly ineffective, to the point that they’re barely more effective than placebos, if at all, and should never have been approved by the FDA (2, 3, 4, 5, 6, 7). This is almost unequivocal in the research, which is quite surprising considering the persistent mainstream narrative about the effectiveness of these drugs and how universally they’re prescribed.

Their lack of effectiveness is nicely summed up in this quote:

Antidepressants are supposed to work by fixing a chemical imbalance, specifically, a lack of serotonin in the brain. Indeed, their supposed effectiveness is the primary evidence for the chemical imbalance theory. But analyses of the published data and the unpublished data that were hidden by drug companies reveals that most (if not all) of the benefits are due to the placebo effect. Some antidepressants increase serotonin levels, some decrease it, and some have no effect at all on serotonin. Nevertheless, they all show the same therapeutic benefit. Even the small statistical difference between antidepressants and placebos may be an enhanced placebo effect, due to the fact that most patients and doctors in clinical trials successfully break blind. The serotonin theory is as close as any theory in the history of science to having been proved wrong. Instead of curing depression, popular antidepressants may induce a biological vulnerability making people more likely to become depressed in the future.” (3) (emphasis mine)

And these drugs are not without side effects. They’ve been shown to cause sexual dysfunction, weight gain, complications during pregnancy, insomnia, apathy and emotional blunting, increases in suicidal ideation and attempts, increases in violent and aggressive behavior, and many other “side effects” (3, 6, 8, 9, 10, 11, 12, 13). They also increase the risk of becoming depressed again and can cause severe withdrawal symptoms when stopped (3, 8, 14, 15).

Due to their lack of effectiveness and side effects, studies have shown that very few people treated with antidepressant medications stick to the treatment (15) and the outcomes of people using antidepressants are worse than those who aren’t treated with antidepressants (5, 16).

Considering their lack of effectiveness, dangerous side effects, and the presence of other treatments that work just as well (if not better), you could even say that it’s irresponsible to continue to sell and prescribe these “antidepressant” medications, as is suggested in this quote:

When different treatments are equally effective, choice should be based on risk and harm, and of all of [the available] treatments, antidepressant drugs are the riskiest and most harmful. If they are to be used at all, it should be as a last resort, when depression is extremely severe and all other treatment alternatives have been tried and failed.” (3)

I don’t think it’s much of a stretch to claim that, as several researchers have suggested, the prescription of these drugs is the result of a triumph of marketing over science, which is evidenced even by the name “antidepressant”:

One day we may look back and marvel at the stroke of marketing genius that led to calling these medications antidepressants in the first place. Kirsch et al. (2002) have demonstrated that just because a pill is called an antidepressant, it doesn’t necessarily make it so.” (17)

Not only does this evidence show that [antidepressant] drugs are little different from placebo, but also that there are no grounds to believe they have specific effects that would justify their classification as ‘antidepressants’” (6)

Regarding SSRIs, there is a growing body of medical literature casting doubt on the serotonin hypothesis, and this body is not reflected in the consumer advertisements. In particular, many SSRI advertisements continue to claim that the mechanism of action of SSRIs is that of correcting a chemical imbalance… Yet, as previously mentioned, there is no such thing as a scientifically established correct “balance” of serotonin. The take-home message for consumers viewing SSRI advertisements is probably that SSRIs work by normalizing neurotransmitters that have gone awry. This was a hopeful notion 30 years ago, but is not an accurate reflection of present-day scientific evidence.“The incongruence between the scientific literature and the claims made in FDA-regulated SSRI advertisements is remarkable, and possibly unparalleled.” (1) (emphasis mine)

It’s quite clear that the chemical imbalance theory has been discredited, yet the damaging effects of this theory stretch beyond the abysmal failure of antidepressant medications.

“Side Effects” of the Chemical Imbalance Theory

There’s another problem with this theory beyond it being completely inaccurate and leading to the prescription of treatments that don’t work.

The idea that our thoughts, mood, and general happiness are determined by chemical imbalances that we have absolutely no control over fosters helplessness. It takes away our power to improve our mental health and encourages us to rely on ineffective medications.

These effects have been shown in studies where patients have been told that their mental health disorders are due to chemical imbalances:

The group who was told they had abnormal serotonin levels found medication more credible than psychotherapy and expected it to be more effective. They also had more pessimism about their prognosis and a lower perceived ability to regulate negative mood states, yet experienced no reduction in self-blame.” (18) (emphasis mine)

This sort of helplessness only makes conditions like depression worse by encouraging the feeling that nothing can be done to improve our thoughts, mood, and perception. But that couldn’t be farther from the truth!

What Can We Do About Depression?

Before I begin explaining what can be done to improve or alleviate depression and other mental health disorders, I want to emphasize that I’m not suggesting that these conditions don’t have a physiological basis, that we should blame ourselves for having them, or that they’re simply “behaviorally-based.”

What I am suggesting is that we aren’t powerless or helpless in these situations. As I mentioned earlier, it’s completely illogical to create a separation between our environment and our mental health as if they aren’t directly interdependent. So, there are things that we can do that directly affect the biological underpinnings that affect our thoughts, mood, and perception.

Let’s first consider that depression and other mental health disorders are, in essence, a result of chronic stress. And by chronic stress, I’m not referring to psychological stress, but rather physiological stress.

Physiological stress is a product of a lack of energy, where our energy demands are greater than our energy supply. And, it’s been shown that this stress, or lack of energy, directly affects our feelings of well-being and causes a physiological response that we consider “depression,” as well as other mental health disorders (19, 20, 21, 22, 23, 24, 25, 26, 27, 28).

But, addressing this energy deficiency can be rather tricky, as it’s affected by all aspects of our environment.

This includes psychological stress, social interaction and relationships, leisure, and loneliness, all of which directly affect our health and well-being (29, 30, 31, 32, 33, 34). This may not be all that surprising, as these are the environmental factors most commonly considered when it comes to mental health disorders.

However, when mental health disorders are reduced to simple chemical imbalances these factors may be ignored. Considering that these aspects of our environment have direct effects on the physiological factors that affect our mental health, ignoring these factors would be a costly mistake.

Other factors like exercise and nutrition also play a major role. It’s widely recognized that these facets of our environment affect our health, but their powerful effects on our thoughts, mood, and sense of well-being are often ignored.

Considering that the psychological aspects of our health are directly influenced by energy balance, it’s imperative that we address the factors affecting our production and usage of energy if we want to improve depression and other mental health disorders. To learn more about how you can address these factors, sign up below for a free 6-day email mini-course on depression, health, and energy balance.

References

Is Depression Really Caused By A Chemical Imbalance?

I know this is a touchy subject.

Not only is mental health a very personal issue, but there’s a stigma surrounding mental health disorders that often comes in the form of blaming those who have these issues or even discounting the legitimacy of these disorders.

And, those who aren’t in favor of the chemical imbalance theory often get lumped in with the people who stigmatize these disorders. Because of these associations, I want to first clarify that I’m NOT blaming anyone for their state of mental health nor am I discounting that these conditions are legitimate and biological in nature.

With that out of the way, we can talk about what’s really causing mental health disorders like depression.

The mainstream belief is that these conditions are caused by specific chemical imbalances in the brain and that these imbalances can only be fixed with prescription medications. This is also known as the “chemical imbalance theory.”

This theory has, in part, led to a dramatic rise in the prescription of antidepressant medications over the past few decades, to the point that over 10% of Americans are taking antidepressants. It has also fueled the massive growth of the multi-billion-dollar antidepressant drug industry.

But, this mainstream theory doesn’t hold up and these medications are not the solution to the growing problem of depression and other mental health disorders.

The Many Flaws of The Chemical Imbalance Theory

First, I’d like to make it clear that I’m not suggesting that the chemicals in our brains don’t affect our mental health. In fact, I would go as far as to say the exact opposite: our mental health and physical health are inextricably linked to the point that there really is no separation – our mental health isn’t at all distinct from our physiology.

And this leads us to one of the biggest flaws of the chemical imbalance theory, which is that the hormones and neurotransmitters that affect our mental health aren’t affected by what’s going on in the rest of our body.

The idea that our mind is separate from our body is extremely common. It’s assumed that our thoughts, mood, and outlook on life are completely independent of the foods we eat, chemicals we’re exposed to, sunlight we get, and all other factors of our environment. But this isn’t at all the case.

There’s no true separation between our mind and body. All these environmental factors affect us on a physiological level, and this includes affecting the many aspects of brain physiology that are related to our thoughts, mood, and perspective through which we see the world. This includes effects on our “brain chemicals,” like serotonin, dopamine, GABA, and norepinephrine.

So the issue isn’t determining whether chemicals in our brain affect our thoughts or mood, the issue is the thinking that these chemicals can’t be changed by our environment and instead are, presumably, primarily genetically determined. This then suggests that there’s nothing we can do about these “chemical imbalances” other than fixing them with prescription medications.

Along with this misconception is the fallacy that mental health disorders as complex as depression can be broken down to simple chemical imbalances (too little or too much of a single neurotransmitter, for example), which is what the antidepressant medications are aimed at treating.

Perhaps surprisingly, these flaws have been extensively acknowledged in the scientific literature:

While neuroscience is a rapidly advancing field, to propose that researchers can objectively identify a “chemical imbalance” at the molecular level is not compatible with the extant science. In fact, there is no scientifically established ideal “chemical balance” of serotonin, let alone an identifiable pathological imbalance. To equate the impressive recent achievements of neuroscience with support for the serotonin hypothesis is a mistake.” (1)

In short, there exists no rigorous corroboration of the serotonin theory, and a significant body of contradictory evidence. Far from being a radical line of thought, doubts about the serotonin hypothesis are well acknowledged by many researchers, including frank statements from prominent psychiatrists, some of whom are even enthusiastic proponents of SSRI medications.” (1)

Nonetheless, the chemical imbalance theory is still the popular narrative outside of the scientific literature. While this theory is heavily flawed, it wouldn’t be nearly as dangerous if the prescribed medications were actually safe and effective.

Antidepressants are some of the most prescribed drugs in the United States, the most common of which are SSRIs. These medications are based on the idea that depression is caused by a lack of serotonin, a notion that has become so pervasive that serotonin is colloquially considered the “happy hormone.” Simply put, this is absolutely not the case, but I’ll dig into that in more detail another time. For now, the complete failure of these drugs will have to do as evidence against this supposition.

Antidepressant drugs are incredibly ineffective, to the point that they’re barely more effective than placebos, if at all, and should never have been approved by the FDA (2, 3, 4, 5, 6, 7). This is almost unequivocal in the research, which is quite surprising considering the persistent mainstream narrative about the effectiveness of these drugs and how universally they’re prescribed.

Their lack of effectiveness is nicely summed up in this quote:

Antidepressants are supposed to work by fixing a chemical imbalance, specifically, a lack of serotonin in the brain. Indeed, their supposed effectiveness is the primary evidence for the chemical imbalance theory. But analyses of the published data and the unpublished data that were hidden by drug companies reveals that most (if not all) of the benefits are due to the placebo effect. Some antidepressants increase serotonin levels, some decrease it, and some have no effect at all on serotonin. Nevertheless, they all show the same therapeutic benefit. Even the small statistical difference between antidepressants and placebos may be an enhanced placebo effect, due to the fact that most patients and doctors in clinical trials successfully break blind. The serotonin theory is as close as any theory in the history of science to having been proved wrong. Instead of curing depression, popular antidepressants may induce a biological vulnerability making people more likely to become depressed in the future.” (3) (emphasis mine)

And these drugs are not without side effects. They’ve been shown to cause sexual dysfunction, weight gain, complications during pregnancy, insomnia, apathy and emotional blunting, increases in suicidal ideation and attempts, increases in violent and aggressive behavior, and many other “side effects” (3, 6, 8, 9, 10, 11, 12, 13). They also increase the risk of becoming depressed again and can cause severe withdrawal symptoms when stopped (3, 8, 14, 15).

Due to their lack of effectiveness and side effects, studies have shown that very few people treated with antidepressant medications stick to the treatment (15) and the outcomes of people using antidepressants are worse than those who aren’t treated with antidepressants (5, 16).

Considering their lack of effectiveness, dangerous side effects, and the presence of other treatments that work just as well (if not better), you could even say that it’s irresponsible to continue to sell and prescribe these “antidepressant” medications, as is suggested in this quote:

When different treatments are equally effective, choice should be based on risk and harm, and of all of [the available] treatments, antidepressant drugs are the riskiest and most harmful. If they are to be used at all, it should be as a last resort, when depression is extremely severe and all other treatment alternatives have been tried and failed.” (3)

I don’t think it’s much of a stretch to claim that, as several researchers have suggested, the prescription of these drugs is the result of a triumph of marketing over science, which is evidenced even by the name “antidepressant”:

One day we may look back and marvel at the stroke of marketing genius that led to calling these medications antidepressants in the first place. Kirsch et al. (2002) have demonstrated that just because a pill is called an antidepressant, it doesn’t necessarily make it so.” (17)

Not only does this evidence show that [antidepressant] drugs are little different from placebo, but also that there are no grounds to believe they have specific effects that would justify their classification as ‘antidepressants’” (6)

Regarding SSRIs, there is a growing body of medical literature casting doubt on the serotonin hypothesis, and this body is not reflected in the consumer advertisements. In particular, many SSRI advertisements continue to claim that the mechanism of action of SSRIs is that of correcting a chemical imbalance… Yet, as previously mentioned, there is no such thing as a scientifically established correct “balance” of serotonin. The take-home message for consumers viewing SSRI advertisements is probably that SSRIs work by normalizing neurotransmitters that have gone awry. This was a hopeful notion 30 years ago, but is not an accurate reflection of present-day scientific evidence.“The incongruence between the scientific literature and the claims made in FDA-regulated SSRI advertisements is remarkable, and possibly unparalleled.” (1) (emphasis mine)

It’s quite clear that the chemical imbalance theory has been discredited, yet the damaging effects of this theory stretch beyond the abysmal failure of antidepressant medications.

“Side Effects” of the Chemical Imbalance Theory

There’s another problem with this theory beyond it being completely inaccurate and leading to the prescription of treatments that don’t work.

The idea that our thoughts, mood, and general happiness are determined by chemical imbalances that we have absolutely no control over fosters helplessness. It takes away our power to improve our mental health and encourages us to rely on ineffective medications.

These effects have been shown in studies where patients have been told that their mental health disorders are due to chemical imbalances:

The group who was told they had abnormal serotonin levels found medication more credible than psychotherapy and expected it to be more effective. They also had more pessimism about their prognosis and a lower perceived ability to regulate negative mood states, yet experienced no reduction in self-blame.” (18) (emphasis mine)

This sort of helplessness only makes conditions like depression worse by encouraging the feeling that nothing can be done to improve our thoughts, mood, and perception. But that couldn’t be farther from the truth!

What Can We Do About Depression?

Before I begin explaining what can be done to improve or alleviate depression and other mental health disorders, I want to emphasize that I’m not suggesting that these conditions don’t have a physiological basis, that we should blame ourselves for having them, or that they’re simply “behaviorally-based.”

What I am suggesting is that we aren’t powerless or helpless in these situations. As I mentioned earlier, it’s completely illogical to create a separation between our environment and our mental health as if they aren’t directly interdependent. So, there are things that we can do that directly affect the biological underpinnings that affect our thoughts, mood, and perception.

Let’s first consider that depression and other mental health disorders are, in essence, a result of chronic stress. And by chronic stress, I’m not referring to psychological stress, but rather physiological stress.

Physiological stress is a product of a lack of energy, where our energy demands are greater than our energy supply. And, it’s been shown that this stress, or lack of energy, directly affects our feelings of well-being and causes a physiological response that we consider “depression,” as well as other mental health disorders (19, 20, 21, 22, 23, 24, 25, 26, 27, 28).

But, addressing this energy deficiency can be rather tricky, as it’s affected by all aspects of our environment.

This includes psychological stress, social interaction and relationships, leisure, and loneliness, all of which directly affect our health and well-being (29, 30, 31, 32, 33, 34). This may not be all that surprising, as these are the environmental factors most commonly considered when it comes to mental health disorders.

However, when mental health disorders are reduced to simple chemical imbalances these factors may be ignored. Considering that these aspects of our environment have direct effects on the physiological factors that affect our mental health, ignoring these factors would be a costly mistake.

Other factors like exercise and nutrition also play a major role. It’s widely recognized that these facets of our environment affect our health, but their powerful effects on our thoughts, mood, and sense of well-being are often ignored.

Considering that the psychological aspects of our health are directly influenced by energy balance, it’s imperative that we address the factors affecting our production and usage of energy if we want to improve depression and other mental health disorders. To learn more about how you can address these factors, sign up below for a free 6-day email mini-course on depression, health, and energy balance.

References

Is Depression Really Caused By A Chemical Imbalance?

I know this is a touchy subject.

Not only is mental health a very personal issue, but there’s a stigma surrounding mental health disorders that often comes in the form of blaming those who have these issues or even discounting the legitimacy of these disorders.

And, those who aren’t in favor of the chemical imbalance theory often get lumped in with the people who stigmatize these disorders. Because of these associations, I want to first clarify that I’m NOT blaming anyone for their state of mental health nor am I discounting that these conditions are legitimate and biological in nature.

With that out of the way, we can talk about what’s really causing mental health disorders like depression.

The mainstream belief is that these conditions are caused by specific chemical imbalances in the brain and that these imbalances can only be fixed with prescription medications. This is also known as the “chemical imbalance theory.”

This theory has, in part, led to a dramatic rise in the prescription of antidepressant medications over the past few decades, to the point that over 10% of Americans are taking antidepressants. It has also fueled the massive growth of the multi-billion-dollar antidepressant drug industry.

But, this mainstream theory doesn’t hold up and these medications are not the solution to the growing problem of depression and other mental health disorders.

The Many Flaws of The Chemical Imbalance Theory

First, I’d like to make it clear that I’m not suggesting that the chemicals in our brains don’t affect our mental health. In fact, I would go as far as to say the exact opposite: our mental health and physical health are inextricably linked to the point that there really is no separation – our mental health isn’t at all distinct from our physiology.

And this leads us to one of the biggest flaws of the chemical imbalance theory, which is that the hormones and neurotransmitters that affect our mental health aren’t affected by what’s going on in the rest of our body.

The idea that our mind is separate from our body is extremely common. It’s assumed that our thoughts, mood, and outlook on life are completely independent of the foods we eat, chemicals we’re exposed to, sunlight we get, and all other factors of our environment. But this isn’t at all the case.

There’s no true separation between our mind and body. All these environmental factors affect us on a physiological level, and this includes affecting the many aspects of brain physiology that are related to our thoughts, mood, and perspective through which we see the world. This includes effects on our “brain chemicals,” like serotonin, dopamine, GABA, and norepinephrine.

So the issue isn’t determining whether chemicals in our brain affect our thoughts or mood, the issue is the thinking that these chemicals can’t be changed by our environment and instead are, presumably, primarily genetically determined. This then suggests that there’s nothing we can do about these “chemical imbalances” other than fixing them with prescription medications.

Along with this misconception is the fallacy that mental health disorders as complex as depression can be broken down to simple chemical imbalances (too little or too much of a single neurotransmitter, for example), which is what the antidepressant medications are aimed at treating.

Perhaps surprisingly, these flaws have been extensively acknowledged in the scientific literature:

While neuroscience is a rapidly advancing field, to propose that researchers can objectively identify a “chemical imbalance” at the molecular level is not compatible with the extant science. In fact, there is no scientifically established ideal “chemical balance” of serotonin, let alone an identifiable pathological imbalance. To equate the impressive recent achievements of neuroscience with support for the serotonin hypothesis is a mistake.” (1)

In short, there exists no rigorous corroboration of the serotonin theory, and a significant body of contradictory evidence. Far from being a radical line of thought, doubts about the serotonin hypothesis are well acknowledged by many researchers, including frank statements from prominent psychiatrists, some of whom are even enthusiastic proponents of SSRI medications.” (1)

Nonetheless, the chemical imbalance theory is still the popular narrative outside of the scientific literature. While this theory is heavily flawed, it wouldn’t be nearly as dangerous if the prescribed medications were actually safe and effective.

Antidepressants are some of the most prescribed drugs in the United States, the most common of which are SSRIs. These medications are based on the idea that depression is caused by a lack of serotonin, a notion that has become so pervasive that serotonin is colloquially considered the “happy hormone.” Simply put, this is absolutely not the case, but I’ll dig into that in more detail another time. For now, the complete failure of these drugs will have to do as evidence against this supposition.

Antidepressant drugs are incredibly ineffective, to the point that they’re barely more effective than placebos, if at all, and should never have been approved by the FDA (2, 3, 4, 5, 6, 7). This is almost unequivocal in the research, which is quite surprising considering the persistent mainstream narrative about the effectiveness of these drugs and how universally they’re prescribed.

Their lack of effectiveness is nicely summed up in this quote:

Antidepressants are supposed to work by fixing a chemical imbalance, specifically, a lack of serotonin in the brain. Indeed, their supposed effectiveness is the primary evidence for the chemical imbalance theory. But analyses of the published data and the unpublished data that were hidden by drug companies reveals that most (if not all) of the benefits are due to the placebo effect. Some antidepressants increase serotonin levels, some decrease it, and some have no effect at all on serotonin. Nevertheless, they all show the same therapeutic benefit. Even the small statistical difference between antidepressants and placebos may be an enhanced placebo effect, due to the fact that most patients and doctors in clinical trials successfully break blind. The serotonin theory is as close as any theory in the history of science to having been proved wrong. Instead of curing depression, popular antidepressants may induce a biological vulnerability making people more likely to become depressed in the future.” (3) (emphasis mine)

And these drugs are not without side effects. They’ve been shown to cause sexual dysfunction, weight gain, complications during pregnancy, insomnia, apathy and emotional blunting, increases in suicidal ideation and attempts, increases in violent and aggressive behavior, and many other “side effects” (3, 6, 8, 9, 10, 11, 12, 13). They also increase the risk of becoming depressed again and can cause severe withdrawal symptoms when stopped (3, 8, 14, 15).

Due to their lack of effectiveness and side effects, studies have shown that very few people treated with antidepressant medications stick to the treatment (15) and the outcomes of people using antidepressants are worse than those who aren’t treated with antidepressants (5, 16).

Considering their lack of effectiveness, dangerous side effects, and the presence of other treatments that work just as well (if not better), you could even say that it’s irresponsible to continue to sell and prescribe these “antidepressant” medications, as is suggested in this quote:

When different treatments are equally effective, choice should be based on risk and harm, and of all of [the available] treatments, antidepressant drugs are the riskiest and most harmful. If they are to be used at all, it should be as a last resort, when depression is extremely severe and all other treatment alternatives have been tried and failed.” (3)

I don’t think it’s much of a stretch to claim that, as several researchers have suggested, the prescription of these drugs is the result of a triumph of marketing over science, which is evidenced even by the name “antidepressant”:

One day we may look back and marvel at the stroke of marketing genius that led to calling these medications antidepressants in the first place. Kirsch et al. (2002) have demonstrated that just because a pill is called an antidepressant, it doesn’t necessarily make it so.” (17)

Not only does this evidence show that [antidepressant] drugs are little different from placebo, but also that there are no grounds to believe they have specific effects that would justify their classification as ‘antidepressants’” (6)

Regarding SSRIs, there is a growing body of medical literature casting doubt on the serotonin hypothesis, and this body is not reflected in the consumer advertisements. In particular, many SSRI advertisements continue to claim that the mechanism of action of SSRIs is that of correcting a chemical imbalance… Yet, as previously mentioned, there is no such thing as a scientifically established correct “balance” of serotonin. The take-home message for consumers viewing SSRI advertisements is probably that SSRIs work by normalizing neurotransmitters that have gone awry. This was a hopeful notion 30 years ago, but is not an accurate reflection of present-day scientific evidence.“The incongruence between the scientific literature and the claims made in FDA-regulated SSRI advertisements is remarkable, and possibly unparalleled.” (1) (emphasis mine)

It’s quite clear that the chemical imbalance theory has been discredited, yet the damaging effects of this theory stretch beyond the abysmal failure of antidepressant medications.

“Side Effects” of the Chemical Imbalance Theory

There’s another problem with this theory beyond it being completely inaccurate and leading to the prescription of treatments that don’t work.

The idea that our thoughts, mood, and general happiness are determined by chemical imbalances that we have absolutely no control over fosters helplessness. It takes away our power to improve our mental health and encourages us to rely on ineffective medications.

These effects have been shown in studies where patients have been told that their mental health disorders are due to chemical imbalances:

The group who was told they had abnormal serotonin levels found medication more credible than psychotherapy and expected it to be more effective. They also had more pessimism about their prognosis and a lower perceived ability to regulate negative mood states, yet experienced no reduction in self-blame.” (18) (emphasis mine)

This sort of helplessness only makes conditions like depression worse by encouraging the feeling that nothing can be done to improve our thoughts, mood, and perception. But that couldn’t be farther from the truth!

What Can We Do About Depression?

Before I begin explaining what can be done to improve or alleviate depression and other mental health disorders, I want to emphasize that I’m not suggesting that these conditions don’t have a physiological basis, that we should blame ourselves for having them, or that they’re simply “behaviorally-based.”

What I am suggesting is that we aren’t powerless or helpless in these situations. As I mentioned earlier, it’s completely illogical to create a separation between our environment and our mental health as if they aren’t directly interdependent. So, there are things that we can do that directly affect the biological underpinnings that affect our thoughts, mood, and perception.

Let’s first consider that depression and other mental health disorders are, in essence, a result of chronic stress. And by chronic stress, I’m not referring to psychological stress, but rather physiological stress.

Physiological stress is a product of a lack of energy, where our energy demands are greater than our energy supply. And, it’s been shown that this stress, or lack of energy, directly affects our feelings of well-being and causes a physiological response that we consider “depression,” as well as other mental health disorders (19, 20, 21, 22, 23, 24, 25, 26, 27, 28).

But, addressing this energy deficiency can be rather tricky, as it’s affected by all aspects of our environment.

This includes psychological stress, social interaction and relationships, leisure, and loneliness, all of which directly affect our health and well-being (29, 30, 31, 32, 33, 34). This may not be all that surprising, as these are the environmental factors most commonly considered when it comes to mental health disorders.

However, when mental health disorders are reduced to simple chemical imbalances these factors may be ignored. Considering that these aspects of our environment have direct effects on the physiological factors that affect our mental health, ignoring these factors would be a costly mistake.

Other factors like exercise and nutrition also play a major role. It’s widely recognized that these facets of our environment affect our health, but their powerful effects on our thoughts, mood, and sense of well-being are often ignored.

Considering that the psychological aspects of our health are directly influenced by energy balance, it’s imperative that we address the factors affecting our production and usage of energy if we want to improve depression and other mental health disorders. To learn more about how you can address these factors, sign up below for a free 6-day email mini-course on depression, health, and energy balance.

References

Is Depression Really Caused By A Chemical Imbalance?

I know this is a touchy subject.

Not only is mental health a very personal issue, but there’s a stigma surrounding mental health disorders that often comes in the form of blaming those who have these issues or even discounting the legitimacy of these disorders.

And, those who aren’t in favor of the chemical imbalance theory often get lumped in with the people who stigmatize these disorders. Because of these associations, I want to first clarify that I’m NOT blaming anyone for their state of mental health nor am I discounting that these conditions are legitimate and biological in nature.

With that out of the way, we can talk about what’s really causing mental health disorders like depression.

The mainstream belief is that these conditions are caused by specific chemical imbalances in the brain and that these imbalances can only be fixed with prescription medications. This is also known as the “chemical imbalance theory.”

This theory has, in part, led to a dramatic rise in the prescription of antidepressant medications over the past few decades, to the point that over 10% of Americans are taking antidepressants. It has also fueled the massive growth of the multi-billion-dollar antidepressant drug industry.

But, this mainstream theory doesn’t hold up and these medications are not the solution to the growing problem of depression and other mental health disorders.

The Many Flaws of The Chemical Imbalance Theory

First, I’d like to make it clear that I’m not suggesting that the chemicals in our brains don’t affect our mental health. In fact, I would go as far as to say the exact opposite: our mental health and physical health are inextricably linked to the point that there really is no separation – our mental health isn’t at all distinct from our physiology.

And this leads us to one of the biggest flaws of the chemical imbalance theory, which is that the hormones and neurotransmitters that affect our mental health aren’t affected by what’s going on in the rest of our body.

The idea that our mind is separate from our body is extremely common. It’s assumed that our thoughts, mood, and outlook on life are completely independent of the foods we eat, chemicals we’re exposed to, sunlight we get, and all other factors of our environment. But this isn’t at all the case.

There’s no true separation between our mind and body. All these environmental factors affect us on a physiological level, and this includes affecting the many aspects of brain physiology that are related to our thoughts, mood, and perspective through which we see the world. This includes effects on our “brain chemicals,” like serotonin, dopamine, GABA, and norepinephrine.

So the issue isn’t determining whether chemicals in our brain affect our thoughts or mood, the issue is the thinking that these chemicals can’t be changed by our environment and instead are, presumably, primarily genetically determined. This then suggests that there’s nothing we can do about these “chemical imbalances” other than fixing them with prescription medications.

Along with this misconception is the fallacy that mental health disorders as complex as depression can be broken down to simple chemical imbalances (too little or too much of a single neurotransmitter, for example), which is what the antidepressant medications are aimed at treating.

Perhaps surprisingly, these flaws have been extensively acknowledged in the scientific literature:

While neuroscience is a rapidly advancing field, to propose that researchers can objectively identify a “chemical imbalance” at the molecular level is not compatible with the extant science. In fact, there is no scientifically established ideal “chemical balance” of serotonin, let alone an identifiable pathological imbalance. To equate the impressive recent achievements of neuroscience with support for the serotonin hypothesis is a mistake.” (1)

In short, there exists no rigorous corroboration of the serotonin theory, and a significant body of contradictory evidence. Far from being a radical line of thought, doubts about the serotonin hypothesis are well acknowledged by many researchers, including frank statements from prominent psychiatrists, some of whom are even enthusiastic proponents of SSRI medications.” (1)

Nonetheless, the chemical imbalance theory is still the popular narrative outside of the scientific literature. While this theory is heavily flawed, it wouldn’t be nearly as dangerous if the prescribed medications were actually safe and effective.

Antidepressants are some of the most prescribed drugs in the United States, the most common of which are SSRIs. These medications are based on the idea that depression is caused by a lack of serotonin, a notion that has become so pervasive that serotonin is colloquially considered the “happy hormone.” Simply put, this is absolutely not the case, but I’ll dig into that in more detail another time. For now, the complete failure of these drugs will have to do as evidence against this supposition.

Antidepressant drugs are incredibly ineffective, to the point that they’re barely more effective than placebos, if at all, and should never have been approved by the FDA (2, 3, 4, 5, 6, 7). This is almost unequivocal in the research, which is quite surprising considering the persistent mainstream narrative about the effectiveness of these drugs and how universally they’re prescribed.

Their lack of effectiveness is nicely summed up in this quote:

Antidepressants are supposed to work by fixing a chemical imbalance, specifically, a lack of serotonin in the brain. Indeed, their supposed effectiveness is the primary evidence for the chemical imbalance theory. But analyses of the published data and the unpublished data that were hidden by drug companies reveals that most (if not all) of the benefits are due to the placebo effect. Some antidepressants increase serotonin levels, some decrease it, and some have no effect at all on serotonin. Nevertheless, they all show the same therapeutic benefit. Even the small statistical difference between antidepressants and placebos may be an enhanced placebo effect, due to the fact that most patients and doctors in clinical trials successfully break blind. The serotonin theory is as close as any theory in the history of science to having been proved wrong. Instead of curing depression, popular antidepressants may induce a biological vulnerability making people more likely to become depressed in the future.” (3) (emphasis mine)

And these drugs are not without side effects. They’ve been shown to cause sexual dysfunction, weight gain, complications during pregnancy, insomnia, apathy and emotional blunting, increases in suicidal ideation and attempts, increases in violent and aggressive behavior, and many other “side effects” (3, 6, 8, 9, 10, 11, 12, 13). They also increase the risk of becoming depressed again and can cause severe withdrawal symptoms when stopped (3, 8, 14, 15).

Due to their lack of effectiveness and side effects, studies have shown that very few people treated with antidepressant medications stick to the treatment (15) and the outcomes of people using antidepressants are worse than those who aren’t treated with antidepressants (5, 16).

Considering their lack of effectiveness, dangerous side effects, and the presence of other treatments that work just as well (if not better), you could even say that it’s irresponsible to continue to sell and prescribe these “antidepressant” medications, as is suggested in this quote:

When different treatments are equally effective, choice should be based on risk and harm, and of all of [the available] treatments, antidepressant drugs are the riskiest and most harmful. If they are to be used at all, it should be as a last resort, when depression is extremely severe and all other treatment alternatives have been tried and failed.” (3)

I don’t think it’s much of a stretch to claim that, as several researchers have suggested, the prescription of these drugs is the result of a triumph of marketing over science, which is evidenced even by the name “antidepressant”:

One day we may look back and marvel at the stroke of marketing genius that led to calling these medications antidepressants in the first place. Kirsch et al. (2002) have demonstrated that just because a pill is called an antidepressant, it doesn’t necessarily make it so.” (17)

Not only does this evidence show that [antidepressant] drugs are little different from placebo, but also that there are no grounds to believe they have specific effects that would justify their classification as ‘antidepressants’” (6)

Regarding SSRIs, there is a growing body of medical literature casting doubt on the serotonin hypothesis, and this body is not reflected in the consumer advertisements. In particular, many SSRI advertisements continue to claim that the mechanism of action of SSRIs is that of correcting a chemical imbalance… Yet, as previously mentioned, there is no such thing as a scientifically established correct “balance” of serotonin. The take-home message for consumers viewing SSRI advertisements is probably that SSRIs work by normalizing neurotransmitters that have gone awry. This was a hopeful notion 30 years ago, but is not an accurate reflection of present-day scientific evidence.“The incongruence between the scientific literature and the claims made in FDA-regulated SSRI advertisements is remarkable, and possibly unparalleled.” (1) (emphasis mine)

It’s quite clear that the chemical imbalance theory has been discredited, yet the damaging effects of this theory stretch beyond the abysmal failure of antidepressant medications.

“Side Effects” of the Chemical Imbalance Theory

There’s another problem with this theory beyond it being completely inaccurate and leading to the prescription of treatments that don’t work.

The idea that our thoughts, mood, and general happiness are determined by chemical imbalances that we have absolutely no control over fosters helplessness. It takes away our power to improve our mental health and encourages us to rely on ineffective medications.

These effects have been shown in studies where patients have been told that their mental health disorders are due to chemical imbalances:

The group who was told they had abnormal serotonin levels found medication more credible than psychotherapy and expected it to be more effective. They also had more pessimism about their prognosis and a lower perceived ability to regulate negative mood states, yet experienced no reduction in self-blame.” (18) (emphasis mine)

This sort of helplessness only makes conditions like depression worse by encouraging the feeling that nothing can be done to improve our thoughts, mood, and perception. But that couldn’t be farther from the truth!

What Can We Do About Depression?

Before I begin explaining what can be done to improve or alleviate depression and other mental health disorders, I want to emphasize that I’m not suggesting that these conditions don’t have a physiological basis, that we should blame ourselves for having them, or that they’re simply “behaviorally-based.”

What I am suggesting is that we aren’t powerless or helpless in these situations. As I mentioned earlier, it’s completely illogical to create a separation between our environment and our mental health as if they aren’t directly interdependent. So, there are things that we can do that directly affect the biological underpinnings that affect our thoughts, mood, and perception.

Let’s first consider that depression and other mental health disorders are, in essence, a result of chronic stress. And by chronic stress, I’m not referring to psychological stress, but rather physiological stress.

Physiological stress is a product of a lack of energy, where our energy demands are greater than our energy supply. And, it’s been shown that this stress, or lack of energy, directly affects our feelings of well-being and causes a physiological response that we consider “depression,” as well as other mental health disorders (19, 20, 21, 22, 23, 24, 25, 26, 27, 28).

But, addressing this energy deficiency can be rather tricky, as it’s affected by all aspects of our environment.

This includes psychological stress, social interaction and relationships, leisure, and loneliness, all of which directly affect our health and well-being (29, 30, 31, 32, 33, 34). This may not be all that surprising, as these are the environmental factors most commonly considered when it comes to mental health disorders.

However, when mental health disorders are reduced to simple chemical imbalances these factors may be ignored. Considering that these aspects of our environment have direct effects on the physiological factors that affect our mental health, ignoring these factors would be a costly mistake.

Other factors like exercise and nutrition also play a major role. It’s widely recognized that these facets of our environment affect our health, but their powerful effects on our thoughts, mood, and sense of well-being are often ignored.

Considering that the psychological aspects of our health are directly influenced by energy balance, it’s imperative that we address the factors affecting our production and usage of energy if we want to improve depression and other mental health disorders. To learn more about how you can address these factors, sign up below for a free 6-day email mini-course on depression, health, and energy balance.

References

Carbs vs. Fats: Hormonal Effects

It’s time to continue the debate on carbs vs. fats.

In the last carbs vs. fats article, I described the different effects of carbohydrates and fats on our health through a bioenergetic lens and how this view suggests that fats are an inferior fuel compared to carbohydrates.

But, many of the claims in favor of “fat-burning,” including that it improves blood sugar regulation, cognitive function, and libido, are directly related to the hormonal effects that result from using fat as the primary fuel source.

As I explained in a recent article, our hormones play an integral role in our adaptive response to our environment and reflect our underlying energetic state. Therefore, changes in fuel availability, or the availability of carbohydrates and fats, have major hormonal effects.

In this article, I’m going to explain exactly how these different fuels affect our hormonal state, specifically in the context of low-carb or ketogenic diets and higher carb diets.

Hormones and Fuel Availability

In my previous article on carbs vs. fats, I explained that fat is our backup fuel, reserved for times when carbohydrates aren’t available, such as in a state of famine or starvation. This is reflected on the energetic level, where using fat for fuel slows the production and usage of energy. And this is also reflected on the hormonal level, which further encourages the conservation of energy in order to prolong survival.

These hormonal effects begin with changes in the availability of glucose. Glucose is our primary fuel source and its availability dictates which fuel will be used to produced energy (1, 2). On a high-carb diet, where the glucose supply is plentiful, glucose is the primary fuel used to produce energy. Whereas on a low-carb or ketogenic diet, or if we don’t eat at all (such as when fasting or if we were starving), there’s reduced glucose availability. Our body then adapts to this situation of reduced glucose availability in several ways.

First, it begins using fats as its primary fuel, which replaces the glucose that would typically be used. However, as I explained in this article, fat is an extremely inefficient fuel, and therefore can’t be used by the brain. So, our bodies will produce glucose to fuel the brain through a process called gluconeogenesis.

Gluconeogenesis takes place in the liver and converts primarily amino acids to glucose. If there isn’t enough protein available from the diet to supply these amino acids, our bodies break down their own muscle tissue or even organ tissue to produce the amino acids needed to produce glucose.

However, regardless of the source of the amino acids, gluconeogenesis is an inefficient and energetically wasteful process (3). So, in addition to producing glucose, our bodies will produce ketones through a process called ketogenesis, which can replace as much as 60% the glucose needed for the brain (4).

All these processes are primarily regulated by the blood sugar regulating hormones, or more accurately, the acute energy regulating hormones.

When carbohydrates aren’t eaten for a few hours, the blood sugar drops which reduces the availability of fuel. This increases the production of glucagon, which leads to the release of glucose from stored glycogen in the liver, as well as the release of fatty acids from fat stores and an increase in fat oxidation.

Then, if carbohydrates still aren’t eaten, the liver will begin to run out of glycogen and adrenaline and cortisol will be released. These hormones cause the breakdown of our tissues and upregulate gluconeogenesis to provide glucose to raise the blood sugar and fuel the brain. They also further increase the usage of fat for fuel while stimulating ketogenesis in order to spare glucose and muscle tissue.

To summarize, when carbohydrates aren’t eaten or if we fast (or starve), our body begins to use primarily fat, our backup fuel, to produce energy while supplying the brain with glucose and ketones through the processes of gluconeogenesis and ketogenesis. These glucose-conserving mechanisms are almost entirely mediated by the stress hormones.

And, these processes are intensified over time on a low-carb or ketogenic diet as the glycogen stores are reduced due to a lack of available glucose, leading to an increased need for fat oxidation, gluconeogenesis, and ketogenesis (5, 6, 7).

As I explained in this article, the stress hormones downregulate our higher-level functions and reduce the production of the prometabolic thyroid and reproductive hormones in order to further conserve energy. These adaptive energy-conserving processes allow us to survive longer when we’re starving or in other extremely stressful situations, which are mimicked by low-carb and ketogenic diets (4, 8, 9).

The opposite occurs on a higher carb diet where blood sugar is effectively regulated. In this case, glucose is supplied by the diet and an adequate glycogen supply, resulting in far less need to use fat for fuel or to stimulate gluconeogenesis or ketogenesis.

So, the amount of stress hormones released to supply fuel is minimal compared to the constant production of stress hormones needed to maintain a fatty acid supply, gluconeogenesis, and ketogenesis on a low-carb or ketogenic diet. And, this difference is even further exaggerated when additional stressors come into play.

Stressors and Fuel Availability

At rest, low-carb and ketogenic diets produce a state where fats become the primary fuel and gluconeogenesis and ketogenesis supply fuel for the brain, basically resulting in constant, low-grade stress. And this effect is intensified even further when stressors are involved.

Stressors, like exercise or psychological stress, increase the energy demand, and therefore the need for additional fuel. The fuel usage hierarchy at rest is mirrored under stress, where glucose is the primary fuel, followed by fat as the backup fuel and ketones as a replacement for some of the glucose needs.

So when we’re faced with stressors on a higher carb diet, the increased fuel needs would mostly be supplied by glycogen, requiring the release of glucagon. Glucagon would also increase the release of fatty acids to supplement this glucose, and any additional fuel needs would be supplied by further increased fat oxidation and eventually gluconeogenesis through the release of adrenaline and cortisol. Glucose could also be supplied by eating carbohydrates, which reduce or completely reverse the stress response, even in severe circumstances (10, 11).

This is contrasted by the stress response that occurs on low-carb and ketogenic diets.

In this case, there’s already little glucose and glycogen available at rest, so fat is the primary fuel used which is largely mediated by the increased production of glucagon and, to a lesser extent, the increased production of adrenaline and cortisol. When faced with additional stressors, greater amounts of adrenaline and cortisol are needed to provide fuel by releasing more fatty acids from fat storage and producing greater amounts of glucose and ketones through gluconeogenesis and ketogenesis.

So, the exposure to stressors on a low-carb or ketogenic diet increases the production of stress hormones to a greater degree than on a higher carb diet (6, 7, 12, 13). This, in turn, leads to an even greater downregulation of our higher-level functions and further reductions in the production of the prometabolic hormones.

In other words, low-carb and ketogenic diets increase the amount of stress hormones produced in response to stressors and reduce our resilience to stress.

What Does This Mean For Our Health?

It’s important to mention that it’s not quite as simple as “carb-burning” vs. “fat-burning.”

Our bodies typically use some combination of carbs and fats as fuel, and this changes based on the time of day, activity level, and other factors. And, this is mirrored by our hormonal profile under these different circumstances.

But, changing the amount of carbohydrates in our diet (such as a higher carb diet vs. a low-carb or ketogenic diet) does have a large effect on which fuel is primarily used and to what extent its favored over the other, as well as on the hormones that regulate these processes. So, a higher carb diet does offer substantial benefits from this perspective.

However it’s also worth noting that, as I explained in my last article on carbs vs. fats, the energetic state produced by a low-carb or ketogenic diet is still better than that produced when both glucose and fat oxidation are inhibited. And the same goes for the hormonal effects.

It’s common for hormonal profiles and related measures and symptoms, like blood sugar regulation, cognitive function, and libido, to improve on low-carb or ketogenic diets when coming from a higher carb diet where both glucose and fat oxidation are inhibited.

But, this doesn’t make these diets ideal. Remember, they still produce a low-energy survival state that leads to adaptive responses (like increased stress hormones and fat and ketone utilization) to conserve energy. In order to attain an optimal, highly energized state, the inhibition of mitochondrial respiration must first be addressed. Then, a higher carb diet can provide the fuel needed to produce an optimal high-energy state and the hormonal state that comes with it.

But remember, this doesn’t mean we need to avoid fat altogether. Fat serves many purposes in our body beyond its use as a fuel source, such as its function as a structural component of our cells and its antimicrobial effects. So, having fat in our diet doesn’t interfere with achieving an optimal high-energy state as long as carbohydrates remain our primary fuel source.

References

Carbs vs. Fats: Hormonal Effects

It’s time to continue the debate on carbs vs. fats.

In the last carbs vs. fats article, I described the different effects of carbohydrates and fats on our health through a bioenergetic lens and how this view suggests that fats are an inferior fuel compared to carbohydrates.

But, many of the claims in favor of “fat-burning,” including that it improves blood sugar regulation, cognitive function, and libido, are directly related to the hormonal effects that result from using fat as the primary fuel source.

As I explained in a recent article, our hormones play an integral role in our adaptive response to our environment and reflect our underlying energetic state. Therefore, changes in fuel availability, or the availability of carbohydrates and fats, have major hormonal effects.

In this article, I’m going to explain exactly how these different fuels affect our hormonal state, specifically in the context of low-carb or ketogenic diets and higher carb diets.

Hormones and Fuel Availability

In my previous article on carbs vs. fats, I explained that fat is our backup fuel, reserved for times when carbohydrates aren’t available, such as in a state of famine or starvation. This is reflected on the energetic level, where using fat for fuel slows the production and usage of energy. And this is also reflected on the hormonal level, which further encourages the conservation of energy in order to prolong survival.

These hormonal effects begin with changes in the availability of glucose. Glucose is our primary fuel source and its availability dictates which fuel will be used to produced energy (1, 2). On a high-carb diet, where the glucose supply is plentiful, glucose is the primary fuel used to produce energy. Whereas on a low-carb or ketogenic diet, or if we don’t eat at all (such as when fasting or if we were starving), there’s reduced glucose availability. Our body then adapts to this situation of reduced glucose availability in several ways.

First, it begins using fats as its primary fuel, which replaces the glucose that would typically be used. However, as I explained in this article, fat is an extremely inefficient fuel, and therefore can’t be used by the brain. So, our bodies will produce glucose to fuel the brain through a process called gluconeogenesis.

Gluconeogenesis takes place in the liver and converts primarily amino acids to glucose. If there isn’t enough protein available from the diet to supply these amino acids, our bodies break down their own muscle tissue or even organ tissue to produce the amino acids needed to produce glucose.

However, regardless of the source of the amino acids, gluconeogenesis is an inefficient and energetically wasteful process (3). So, in addition to producing glucose, our bodies will produce ketones through a process called ketogenesis, which can replace as much as 60% the glucose needed for the brain (4).

All these processes are primarily regulated by the blood sugar regulating hormones, or more accurately, the acute energy regulating hormones.

When carbohydrates aren’t eaten for a few hours, the blood sugar drops which reduces the availability of fuel. This increases the production of glucagon, which leads to the release of glucose from stored glycogen in the liver, as well as the release of fatty acids from fat stores and an increase in fat oxidation.

Then, if carbohydrates still aren’t eaten, the liver will begin to run out of glycogen and adrenaline and cortisol will be released. These hormones cause the breakdown of our tissues and upregulate gluconeogenesis to provide glucose to raise the blood sugar and fuel the brain. They also further increase the usage of fat for fuel while stimulating ketogenesis in order to spare glucose and muscle tissue.

To summarize, when carbohydrates aren’t eaten or if we fast (or starve), our body begins to use primarily fat, our backup fuel, to produce energy while supplying the brain with glucose and ketones through the processes of gluconeogenesis and ketogenesis. These glucose-conserving mechanisms are almost entirely mediated by the stress hormones.

And, these processes are intensified over time on a low-carb or ketogenic diet as the glycogen stores are reduced due to a lack of available glucose, leading to an increased need for fat oxidation, gluconeogenesis, and ketogenesis (5, 6, 7).

As I explained in this article, the stress hormones downregulate our higher-level functions and reduce the production of the prometabolic thyroid and reproductive hormones in order to further conserve energy. These adaptive energy-conserving processes allow us to survive longer when we’re starving or in other extremely stressful situations, which are mimicked by low-carb and ketogenic diets (4, 8, 9).

The opposite occurs on a higher carb diet where blood sugar is effectively regulated. In this case, glucose is supplied by the diet and an adequate glycogen supply, resulting in far less need to use fat for fuel or to stimulate gluconeogenesis or ketogenesis.

So, the amount of stress hormones released to supply fuel is minimal compared to the constant production of stress hormones needed to maintain a fatty acid supply, gluconeogenesis, and ketogenesis on a low-carb or ketogenic diet. And, this difference is even further exaggerated when additional stressors come into play.

Stressors and Fuel Availability

At rest, low-carb and ketogenic diets produce a state where fats become the primary fuel and gluconeogenesis and ketogenesis supply fuel for the brain, basically resulting in constant, low-grade stress. And this effect is intensified even further when stressors are involved.

Stressors, like exercise or psychological stress, increase the energy demand, and therefore the need for additional fuel. The fuel usage hierarchy at rest is mirrored under stress, where glucose is the primary fuel, followed by fat as the backup fuel and ketones as a replacement for some of the glucose needs.

So when we’re faced with stressors on a higher carb diet, the increased fuel needs would mostly be supplied by glycogen, requiring the release of glucagon. Glucagon would also increase the release of fatty acids to supplement this glucose, and any additional fuel needs would be supplied by further increased fat oxidation and eventually gluconeogenesis through the release of adrenaline and cortisol. Glucose could also be supplied by eating carbohydrates, which reduce or completely reverse the stress response, even in severe circumstances (10, 11).

This is contrasted by the stress response that occurs on low-carb and ketogenic diets.

In this case, there’s already little glucose and glycogen available at rest, so fat is the primary fuel used which is largely mediated by the increased production of glucagon and, to a lesser extent, the increased production of adrenaline and cortisol. When faced with additional stressors, greater amounts of adrenaline and cortisol are needed to provide fuel by releasing more fatty acids from fat storage and producing greater amounts of glucose and ketones through gluconeogenesis and ketogenesis.

So, the exposure to stressors on a low-carb or ketogenic diet increases the production of stress hormones to a greater degree than on a higher carb diet (6, 7, 12, 13). This, in turn, leads to an even greater downregulation of our higher-level functions and further reductions in the production of the prometabolic hormones.

In other words, low-carb and ketogenic diets increase the amount of stress hormones produced in response to stressors and reduce our resilience to stress.

What Does This Mean For Our Health?

It’s important to mention that it’s not quite as simple as “carb-burning” vs. “fat-burning.”

Our bodies typically use some combination of carbs and fats as fuel, and this changes based on the time of day, activity level, and other factors. And, this is mirrored by our hormonal profile under these different circumstances.

But, changing the amount of carbohydrates in our diet (such as a higher carb diet vs. a low-carb or ketogenic diet) does have a large effect on which fuel is primarily used and to what extent its favored over the other, as well as on the hormones that regulate these processes. So, a higher carb diet does offer substantial benefits from this perspective.

However it’s also worth noting that, as I explained in my last article on carbs vs. fats, the energetic state produced by a low-carb or ketogenic diet is still better than that produced when both glucose and fat oxidation are inhibited. And the same goes for the hormonal effects.

It’s common for hormonal profiles and related measures and symptoms, like blood sugar regulation, cognitive function, and libido, to improve on low-carb or ketogenic diets when coming from a higher carb diet where both glucose and fat oxidation are inhibited.

But, this doesn’t make these diets ideal. Remember, they still produce a low-energy survival state that leads to adaptive responses (like increased stress hormones and fat and ketone utilization) to conserve energy. In order to attain an optimal, highly energized state, the inhibition of mitochondrial respiration must first be addressed. Then, a higher carb diet can provide the fuel needed to produce an optimal high-energy state and the hormonal state that comes with it.

But remember, this doesn’t mean we need to avoid fat altogether. Fat serves many purposes in our body beyond its use as a fuel source, such as its function as a structural component of our cells and its antimicrobial effects. So, having fat in our diet doesn’t interfere with achieving an optimal high-energy state as long as carbohydrates remain our primary fuel source.

References

Carbs vs. Fats: Hormonal Effects

It’s time to continue the debate on carbs vs. fats.

In the last carbs vs. fats article, I described the different effects of carbohydrates and fats on our health through a bioenergetic lens and how this view suggests that fats are an inferior fuel compared to carbohydrates.

But, many of the claims in favor of “fat-burning,” including that it improves blood sugar regulation, cognitive function, and libido, are directly related to the hormonal effects that result from using fat as the primary fuel source.

As I explained in a recent article, our hormones play an integral role in our adaptive response to our environment and reflect our underlying energetic state. Therefore, changes in fuel availability, or the availability of carbohydrates and fats, have major hormonal effects.

In this article, I’m going to explain exactly how these different fuels affect our hormonal state, specifically in the context of low-carb or ketogenic diets and higher carb diets.

Hormones and Fuel Availability

In my previous article on carbs vs. fats, I explained that fat is our backup fuel, reserved for times when carbohydrates aren’t available, such as in a state of famine or starvation. This is reflected on the energetic level, where using fat for fuel slows the production and usage of energy. And this is also reflected on the hormonal level, which further encourages the conservation of energy in order to prolong survival.

These hormonal effects begin with changes in the availability of glucose. Glucose is our primary fuel source and its availability dictates which fuel will be used to produced energy (1, 2). On a high-carb diet, where the glucose supply is plentiful, glucose is the primary fuel used to produce energy. Whereas on a low-carb or ketogenic diet, or if we don’t eat at all (such as when fasting or if we were starving), there’s reduced glucose availability. Our body then adapts to this situation of reduced glucose availability in several ways.

First, it begins using fats as its primary fuel, which replaces the glucose that would typically be used. However, as I explained in this article, fat is an extremely inefficient fuel, and therefore can’t be used by the brain. So, our bodies will produce glucose to fuel the brain through a process called gluconeogenesis.

Gluconeogenesis takes place in the liver and converts primarily amino acids to glucose. If there isn’t enough protein available from the diet to supply these amino acids, our bodies break down their own muscle tissue or even organ tissue to produce the amino acids needed to produce glucose.

However, regardless of the source of the amino acids, gluconeogenesis is an inefficient and energetically wasteful process (3). So, in addition to producing glucose, our bodies will produce ketones through a process called ketogenesis, which can replace as much as 60% the glucose needed for the brain (4).

All these processes are primarily regulated by the blood sugar regulating hormones, or more accurately, the acute energy regulating hormones.

When carbohydrates aren’t eaten for a few hours, the blood sugar drops which reduces the availability of fuel. This increases the production of glucagon, which leads to the release of glucose from stored glycogen in the liver, as well as the release of fatty acids from fat stores and an increase in fat oxidation.

Then, if carbohydrates still aren’t eaten, the liver will begin to run out of glycogen and adrenaline and cortisol will be released. These hormones cause the breakdown of our tissues and upregulate gluconeogenesis to provide glucose to raise the blood sugar and fuel the brain. They also further increase the usage of fat for fuel while stimulating ketogenesis in order to spare glucose and muscle tissue.

To summarize, when carbohydrates aren’t eaten or if we fast (or starve), our body begins to use primarily fat, our backup fuel, to produce energy while supplying the brain with glucose and ketones through the processes of gluconeogenesis and ketogenesis. These glucose-conserving mechanisms are almost entirely mediated by the stress hormones.

And, these processes are intensified over time on a low-carb or ketogenic diet as the glycogen stores are reduced due to a lack of available glucose, leading to an increased need for fat oxidation, gluconeogenesis, and ketogenesis (5, 6, 7).

As I explained in this article, the stress hormones downregulate our higher-level functions and reduce the production of the prometabolic thyroid and reproductive hormones in order to further conserve energy. These adaptive energy-conserving processes allow us to survive longer when we’re starving or in other extremely stressful situations, which are mimicked by low-carb and ketogenic diets (4, 8, 9).

The opposite occurs on a higher carb diet where blood sugar is effectively regulated. In this case, glucose is supplied by the diet and an adequate glycogen supply, resulting in far less need to use fat for fuel or to stimulate gluconeogenesis or ketogenesis.

So, the amount of stress hormones released to supply fuel is minimal compared to the constant production of stress hormones needed to maintain a fatty acid supply, gluconeogenesis, and ketogenesis on a low-carb or ketogenic diet. And, this difference is even further exaggerated when additional stressors come into play.

Stressors and Fuel Availability

At rest, low-carb and ketogenic diets produce a state where fats become the primary fuel and gluconeogenesis and ketogenesis supply fuel for the brain, basically resulting in constant, low-grade stress. And this effect is intensified even further when stressors are involved.

Stressors, like exercise or psychological stress, increase the energy demand, and therefore the need for additional fuel. The fuel usage hierarchy at rest is mirrored under stress, where glucose is the primary fuel, followed by fat as the backup fuel and ketones as a replacement for some of the glucose needs.

So when we’re faced with stressors on a higher carb diet, the increased fuel needs would mostly be supplied by glycogen, requiring the release of glucagon. Glucagon would also increase the release of fatty acids to supplement this glucose, and any additional fuel needs would be supplied by further increased fat oxidation and eventually gluconeogenesis through the release of adrenaline and cortisol. Glucose could also be supplied by eating carbohydrates, which reduce or completely reverse the stress response, even in severe circumstances (10, 11).

This is contrasted by the stress response that occurs on low-carb and ketogenic diets.

In this case, there’s already little glucose and glycogen available at rest, so fat is the primary fuel used which is largely mediated by the increased production of glucagon and, to a lesser extent, the increased production of adrenaline and cortisol. When faced with additional stressors, greater amounts of adrenaline and cortisol are needed to provide fuel by releasing more fatty acids from fat storage and producing greater amounts of glucose and ketones through gluconeogenesis and ketogenesis.

So, the exposure to stressors on a low-carb or ketogenic diet increases the production of stress hormones to a greater degree than on a higher carb diet (6, 7, 12, 13). This, in turn, leads to an even greater downregulation of our higher-level functions and further reductions in the production of the prometabolic hormones.

In other words, low-carb and ketogenic diets increase the amount of stress hormones produced in response to stressors and reduce our resilience to stress.

What Does This Mean For Our Health?

It’s important to mention that it’s not quite as simple as “carb-burning” vs. “fat-burning.”

Our bodies typically use some combination of carbs and fats as fuel, and this changes based on the time of day, activity level, and other factors. And, this is mirrored by our hormonal profile under these different circumstances.

But, changing the amount of carbohydrates in our diet (such as a higher carb diet vs. a low-carb or ketogenic diet) does have a large effect on which fuel is primarily used and to what extent its favored over the other, as well as on the hormones that regulate these processes. So, a higher carb diet does offer substantial benefits from this perspective.

However it’s also worth noting that, as I explained in my last article on carbs vs. fats, the energetic state produced by a low-carb or ketogenic diet is still better than that produced when both glucose and fat oxidation are inhibited. And the same goes for the hormonal effects.

It’s common for hormonal profiles and related measures and symptoms, like blood sugar regulation, cognitive function, and libido, to improve on low-carb or ketogenic diets when coming from a higher carb diet where both glucose and fat oxidation are inhibited.

But, this doesn’t make these diets ideal. Remember, they still produce a low-energy survival state that leads to adaptive responses (like increased stress hormones and fat and ketone utilization) to conserve energy. In order to attain an optimal, highly energized state, the inhibition of mitochondrial respiration must first be addressed. Then, a higher carb diet can provide the fuel needed to produce an optimal high-energy state and the hormonal state that comes with it.

But remember, this doesn’t mean we need to avoid fat altogether. Fat serves many purposes in our body beyond its use as a fuel source, such as its function as a structural component of our cells and its antimicrobial effects. So, having fat in our diet doesn’t interfere with achieving an optimal high-energy state as long as carbohydrates remain our primary fuel source.

References

Carbs vs. Fats: Hormonal Effects

It’s time to continue the debate on carbs vs. fats.

In the last carbs vs. fats article, I described the different effects of carbohydrates and fats on our health through a bioenergetic lens and how this view suggests that fats are an inferior fuel compared to carbohydrates.

But, many of the claims in favor of “fat-burning,” including that it improves blood sugar regulation, cognitive function, and libido, are directly related to the hormonal effects that result from using fat as the primary fuel source.

As I explained in a recent article, our hormones play an integral role in our adaptive response to our environment and reflect our underlying energetic state. Therefore, changes in fuel availability, or the availability of carbohydrates and fats, have major hormonal effects.

In this article, I’m going to explain exactly how these different fuels affect our hormonal state, specifically in the context of low-carb or ketogenic diets and higher carb diets.

Hormones and Fuel Availability

In my previous article on carbs vs. fats, I explained that fat is our backup fuel, reserved for times when carbohydrates aren’t available, such as in a state of famine or starvation. This is reflected on the energetic level, where using fat for fuel slows the production and usage of energy. And this is also reflected on the hormonal level, which further encourages the conservation of energy in order to prolong survival.

These hormonal effects begin with changes in the availability of glucose. Glucose is our primary fuel source and its availability dictates which fuel will be used to produced energy (1, 2). On a high-carb diet, where the glucose supply is plentiful, glucose is the primary fuel used to produce energy. Whereas on a low-carb or ketogenic diet, or if we don’t eat at all (such as when fasting or if we were starving), there’s reduced glucose availability. Our body then adapts to this situation of reduced glucose availability in several ways.

First, it begins using fats as its primary fuel, which replaces the glucose that would typically be used. However, as I explained in this article, fat is an extremely inefficient fuel, and therefore can’t be used by the brain. So, our bodies will produce glucose to fuel the brain through a process called gluconeogenesis.

Gluconeogenesis takes place in the liver and converts primarily amino acids to glucose. If there isn’t enough protein available from the diet to supply these amino acids, our bodies break down their own muscle tissue or even organ tissue to produce the amino acids needed to produce glucose.

However, regardless of the source of the amino acids, gluconeogenesis is an inefficient and energetically wasteful process (3). So, in addition to producing glucose, our bodies will produce ketones through a process called ketogenesis, which can replace as much as 60% the glucose needed for the brain (4).

All these processes are primarily regulated by the blood sugar regulating hormones, or more accurately, the acute energy regulating hormones.

When carbohydrates aren’t eaten for a few hours, the blood sugar drops which reduces the availability of fuel. This increases the production of glucagon, which leads to the release of glucose from stored glycogen in the liver, as well as the release of fatty acids from fat stores and an increase in fat oxidation.

Then, if carbohydrates still aren’t eaten, the liver will begin to run out of glycogen and adrenaline and cortisol will be released. These hormones cause the breakdown of our tissues and upregulate gluconeogenesis to provide glucose to raise the blood sugar and fuel the brain. They also further increase the usage of fat for fuel while stimulating ketogenesis in order to spare glucose and muscle tissue.

To summarize, when carbohydrates aren’t eaten or if we fast (or starve), our body begins to use primarily fat, our backup fuel, to produce energy while supplying the brain with glucose and ketones through the processes of gluconeogenesis and ketogenesis. These glucose-conserving mechanisms are almost entirely mediated by the stress hormones.

And, these processes are intensified over time on a low-carb or ketogenic diet as the glycogen stores are reduced due to a lack of available glucose, leading to an increased need for fat oxidation, gluconeogenesis, and ketogenesis (5, 6, 7).

As I explained in this article, the stress hormones downregulate our higher-level functions and reduce the production of the prometabolic thyroid and reproductive hormones in order to further conserve energy. These adaptive energy-conserving processes allow us to survive longer when we’re starving or in other extremely stressful situations, which are mimicked by low-carb and ketogenic diets (4, 8, 9).

The opposite occurs on a higher carb diet where blood sugar is effectively regulated. In this case, glucose is supplied by the diet and an adequate glycogen supply, resulting in far less need to use fat for fuel or to stimulate gluconeogenesis or ketogenesis.

So, the amount of stress hormones released to supply fuel is minimal compared to the constant production of stress hormones needed to maintain a fatty acid supply, gluconeogenesis, and ketogenesis on a low-carb or ketogenic diet. And, this difference is even further exaggerated when additional stressors come into play.

Stressors and Fuel Availability

At rest, low-carb and ketogenic diets produce a state where fats become the primary fuel and gluconeogenesis and ketogenesis supply fuel for the brain, basically resulting in constant, low-grade stress. And this effect is intensified even further when stressors are involved.

Stressors, like exercise or psychological stress, increase the energy demand, and therefore the need for additional fuel. The fuel usage hierarchy at rest is mirrored under stress, where glucose is the primary fuel, followed by fat as the backup fuel and ketones as a replacement for some of the glucose needs.

So when we’re faced with stressors on a higher carb diet, the increased fuel needs would mostly be supplied by glycogen, requiring the release of glucagon. Glucagon would also increase the release of fatty acids to supplement this glucose, and any additional fuel needs would be supplied by further increased fat oxidation and eventually gluconeogenesis through the release of adrenaline and cortisol. Glucose could also be supplied by eating carbohydrates, which reduce or completely reverse the stress response, even in severe circumstances (10, 11).

This is contrasted by the stress response that occurs on low-carb and ketogenic diets.

In this case, there’s already little glucose and glycogen available at rest, so fat is the primary fuel used which is largely mediated by the increased production of glucagon and, to a lesser extent, the increased production of adrenaline and cortisol. When faced with additional stressors, greater amounts of adrenaline and cortisol are needed to provide fuel by releasing more fatty acids from fat storage and producing greater amounts of glucose and ketones through gluconeogenesis and ketogenesis.

So, the exposure to stressors on a low-carb or ketogenic diet increases the production of stress hormones to a greater degree than on a higher carb diet (6, 7, 12, 13). This, in turn, leads to an even greater downregulation of our higher-level functions and further reductions in the production of the prometabolic hormones.

In other words, low-carb and ketogenic diets increase the amount of stress hormones produced in response to stressors and reduce our resilience to stress.

What Does This Mean For Our Health?

It’s important to mention that it’s not quite as simple as “carb-burning” vs. “fat-burning.”

Our bodies typically use some combination of carbs and fats as fuel, and this changes based on the time of day, activity level, and other factors. And, this is mirrored by our hormonal profile under these different circumstances.

But, changing the amount of carbohydrates in our diet (such as a higher carb diet vs. a low-carb or ketogenic diet) does have a large effect on which fuel is primarily used and to what extent its favored over the other, as well as on the hormones that regulate these processes. So, a higher carb diet does offer substantial benefits from this perspective.

However it’s also worth noting that, as I explained in my last article on carbs vs. fats, the energetic state produced by a low-carb or ketogenic diet is still better than that produced when both glucose and fat oxidation are inhibited. And the same goes for the hormonal effects.

It’s common for hormonal profiles and related measures and symptoms, like blood sugar regulation, cognitive function, and libido, to improve on low-carb or ketogenic diets when coming from a higher carb diet where both glucose and fat oxidation are inhibited.

But, this doesn’t make these diets ideal. Remember, they still produce a low-energy survival state that leads to adaptive responses (like increased stress hormones and fat and ketone utilization) to conserve energy. In order to attain an optimal, highly energized state, the inhibition of mitochondrial respiration must first be addressed. Then, a higher carb diet can provide the fuel needed to produce an optimal high-energy state and the hormonal state that comes with it.

But remember, this doesn’t mean we need to avoid fat altogether. Fat serves many purposes in our body beyond its use as a fuel source, such as its function as a structural component of our cells and its antimicrobial effects. So, having fat in our diet doesn’t interfere with achieving an optimal high-energy state as long as carbohydrates remain our primary fuel source.

References

Carbs vs. Fats: Hormonal Effects

It’s time to continue the debate on carbs vs. fats.

In the last carbs vs. fats article, I described the different effects of carbohydrates and fats on our health through a bioenergetic lens and how this view suggests that fats are an inferior fuel compared to carbohydrates.

But, many of the claims in favor of “fat-burning,” including that it improves blood sugar regulation, cognitive function, and libido, are directly related to the hormonal effects that result from using fat as the primary fuel source.

As I explained in a recent article, our hormones play an integral role in our adaptive response to our environment and reflect our underlying energetic state. Therefore, changes in fuel availability, or the availability of carbohydrates and fats, have major hormonal effects.

In this article, I’m going to explain exactly how these different fuels affect our hormonal state, specifically in the context of low-carb or ketogenic diets and higher carb diets.

Hormones and Fuel Availability

In my previous article on carbs vs. fats, I explained that fat is our backup fuel, reserved for times when carbohydrates aren’t available, such as in a state of famine or starvation. This is reflected on the energetic level, where using fat for fuel slows the production and usage of energy. And this is also reflected on the hormonal level, which further encourages the conservation of energy in order to prolong survival.

These hormonal effects begin with changes in the availability of glucose. Glucose is our primary fuel source and its availability dictates which fuel will be used to produced energy (1, 2). On a high-carb diet, where the glucose supply is plentiful, glucose is the primary fuel used to produce energy. Whereas on a low-carb or ketogenic diet, or if we don’t eat at all (such as when fasting or if we were starving), there’s reduced glucose availability. Our body then adapts to this situation of reduced glucose availability in several ways.

First, it begins using fats as its primary fuel, which replaces the glucose that would typically be used. However, as I explained in this article, fat is an extremely inefficient fuel, and therefore can’t be used by the brain. So, our bodies will produce glucose to fuel the brain through a process called gluconeogenesis.

Gluconeogenesis takes place in the liver and converts primarily amino acids to glucose. If there isn’t enough protein available from the diet to supply these amino acids, our bodies break down their own muscle tissue or even organ tissue to produce the amino acids needed to produce glucose.

However, regardless of the source of the amino acids, gluconeogenesis is an inefficient and energetically wasteful process (3). So, in addition to producing glucose, our bodies will produce ketones through a process called ketogenesis, which can replace as much as 60% the glucose needed for the brain (4).

All these processes are primarily regulated by the blood sugar regulating hormones, or more accurately, the acute energy regulating hormones.

When carbohydrates aren’t eaten for a few hours, the blood sugar drops which reduces the availability of fuel. This increases the production of glucagon, which leads to the release of glucose from stored glycogen in the liver, as well as the release of fatty acids from fat stores and an increase in fat oxidation.

Then, if carbohydrates still aren’t eaten, the liver will begin to run out of glycogen and adrenaline and cortisol will be released. These hormones cause the breakdown of our tissues and upregulate gluconeogenesis to provide glucose to raise the blood sugar and fuel the brain. They also further increase the usage of fat for fuel while stimulating ketogenesis in order to spare glucose and muscle tissue.

To summarize, when carbohydrates aren’t eaten or if we fast (or starve), our body begins to use primarily fat, our backup fuel, to produce energy while supplying the brain with glucose and ketones through the processes of gluconeogenesis and ketogenesis. These glucose-conserving mechanisms are almost entirely mediated by the stress hormones.

And, these processes are intensified over time on a low-carb or ketogenic diet as the glycogen stores are reduced due to a lack of available glucose, leading to an increased need for fat oxidation, gluconeogenesis, and ketogenesis (5, 6, 7).

As I explained in this article, the stress hormones downregulate our higher-level functions and reduce the production of the prometabolic thyroid and reproductive hormones in order to further conserve energy. These adaptive energy-conserving processes allow us to survive longer when we’re starving or in other extremely stressful situations, which are mimicked by low-carb and ketogenic diets (4, 8, 9).

The opposite occurs on a higher carb diet where blood sugar is effectively regulated. In this case, glucose is supplied by the diet and an adequate glycogen supply, resulting in far less need to use fat for fuel or to stimulate gluconeogenesis or ketogenesis.

So, the amount of stress hormones released to supply fuel is minimal compared to the constant production of stress hormones needed to maintain a fatty acid supply, gluconeogenesis, and ketogenesis on a low-carb or ketogenic diet. And, this difference is even further exaggerated when additional stressors come into play.

Stressors and Fuel Availability

At rest, low-carb and ketogenic diets produce a state where fats become the primary fuel and gluconeogenesis and ketogenesis supply fuel for the brain, basically resulting in constant, low-grade stress. And this effect is intensified even further when stressors are involved.

Stressors, like exercise or psychological stress, increase the energy demand, and therefore the need for additional fuel. The fuel usage hierarchy at rest is mirrored under stress, where glucose is the primary fuel, followed by fat as the backup fuel and ketones as a replacement for some of the glucose needs.

So when we’re faced with stressors on a higher carb diet, the increased fuel needs would mostly be supplied by glycogen, requiring the release of glucagon. Glucagon would also increase the release of fatty acids to supplement this glucose, and any additional fuel needs would be supplied by further increased fat oxidation and eventually gluconeogenesis through the release of adrenaline and cortisol. Glucose could also be supplied by eating carbohydrates, which reduce or completely reverse the stress response, even in severe circumstances (10, 11).

This is contrasted by the stress response that occurs on low-carb and ketogenic diets.

In this case, there’s already little glucose and glycogen available at rest, so fat is the primary fuel used which is largely mediated by the increased production of glucagon and, to a lesser extent, the increased production of adrenaline and cortisol. When faced with additional stressors, greater amounts of adrenaline and cortisol are needed to provide fuel by releasing more fatty acids from fat storage and producing greater amounts of glucose and ketones through gluconeogenesis and ketogenesis.

So, the exposure to stressors on a low-carb or ketogenic diet increases the production of stress hormones to a greater degree than on a higher carb diet (6, 7, 12, 13). This, in turn, leads to an even greater downregulation of our higher-level functions and further reductions in the production of the prometabolic hormones.

In other words, low-carb and ketogenic diets increase the amount of stress hormones produced in response to stressors and reduce our resilience to stress.

What Does This Mean For Our Health?

It’s important to mention that it’s not quite as simple as “carb-burning” vs. “fat-burning.”

Our bodies typically use some combination of carbs and fats as fuel, and this changes based on the time of day, activity level, and other factors. And, this is mirrored by our hormonal profile under these different circumstances.

But, changing the amount of carbohydrates in our diet (such as a higher carb diet vs. a low-carb or ketogenic diet) does have a large effect on which fuel is primarily used and to what extent its favored over the other, as well as on the hormones that regulate these processes. So, a higher carb diet does offer substantial benefits from this perspective.

However it’s also worth noting that, as I explained in my last article on carbs vs. fats, the energetic state produced by a low-carb or ketogenic diet is still better than that produced when both glucose and fat oxidation are inhibited. And the same goes for the hormonal effects.

It’s common for hormonal profiles and related measures and symptoms, like blood sugar regulation, cognitive function, and libido, to improve on low-carb or ketogenic diets when coming from a higher carb diet where both glucose and fat oxidation are inhibited.

But, this doesn’t make these diets ideal. Remember, they still produce a low-energy survival state that leads to adaptive responses (like increased stress hormones and fat and ketone utilization) to conserve energy. In order to attain an optimal, highly energized state, the inhibition of mitochondrial respiration must first be addressed. Then, a higher carb diet can provide the fuel needed to produce an optimal high-energy state and the hormonal state that comes with it.

But remember, this doesn’t mean we need to avoid fat altogether. Fat serves many purposes in our body beyond its use as a fuel source, such as its function as a structural component of our cells and its antimicrobial effects. So, having fat in our diet doesn’t interfere with achieving an optimal high-energy state as long as carbohydrates remain our primary fuel source.

References

Hormones: Don’t Shoot The Messengers

Hormones are a common focus when it comes to our health, especially in the alternative field. Hormone imbalances are considered to cause various issues, including hypothyroidism, blood sugar dysregulation, acne, PMS, PCOS, weight gain, mood instability, depression, and many others. As a result, our hormones have become the targets for various interventions.

Foods, supplements, medications, or hormonal replacements are used to “improve our hormonal health” and resolve any of these issues. But, like many other reductionist tendencies, this kind of thinking can lead us astray.

In the same way that our heart doesn’t function independently of our brain or liver or gut, our hormones aren’t a separate, independent feature of our health. In fact, they’re almost exactly the opposite.

Hormones are part of the body’s response to its internal environment. They provide signals based on the environmental conditions, including the availability of energy, which then allows us to best adapt to the circumstances we’re faced with. Because they respond to our internal environment in both the short- and long-term, our hormones are a direct reflection of our general state of health.

In this article, I’m going to shed some light on the adaptive roles of our hormones and how they’re related to our energetic state, while also explaining why interventions aimed at improving hormonal health are often misguided and can distract from the real issues that need to be addressed.

 

Hormones and Energy Balance

In a recent article I explained that energy is the most fundamental force driving our health. It allows every cell in our body to function, and as such is the basic determinant of how well our bodies function.

The amount of energy available to us is dependent on our environment. The amount and type of foods we eat, sunlight exposure, physical and mental activity, and many other factors in our environment determine how much energy our bodies can produce and use.

Our bodies are then designed to adapt to their environment based on the amount of energy available. And this is where the energy-regulating hormones come in.

Our energy-regulating hormones are a major part of this adaptive process. They act as signals that regulate our bodies’ functions based on the amount of energy available.

If there’s a lot of energy available, these hormones will upregulate our energetically expensive functions that allow us to operate optimally. But if there’s not a lot of energy available, these hormones will downregulate these energetically expensive functions in order to conserve energy, kind of like “low-battery mode.”

These changes allow us to survive longer during times of low energy availability and thrive during times of high energy availability.

 

Acute Regulation of Energy Availability

The primary hormones that regulate acute energy availability are glucagon, adrenaline (or epinephrine), and cortisol. These hormones also happen to be the major blood sugar regulating hormones.

This is no accident – as I explained in this article on blood sugar regulation, our blood sugar is one of the most sensitive indicators of our energetic environment as it’s responsible for supplying fuel to our brain and the rest of our bodies.

When energy availability is low, whether it’s due to a lack of fuel (low blood sugar), the inhibition of energy production, or the increased usage of energy, these hormones are released (1). They’re therefore considered to be stress hormones, as they’re produced when the body is under stress due to a lack of energy.

(The categorization of these hormones as “stress hormones” has led to the mistaken idea that these hormones are primarily produced in response to psychological stress, but any stressor can increase the usage of energy, potentially causing the production of these hormones. This includes physical activity such as exercise, as well as mental activity like problem-solving, processing emotions, and what we would consider “psychological stress.”)

In response to this lack of energy, these hormones increase fuel availability by elevating our blood sugar and increasing the production of free fatty acids while also stimulating energy production so that we can deal with the energy deficit at hand (1, 2, 3, 4, 5). They also make us hungry and increase cravings for carbohydrates to increase the availability of fuel (1, 6, 7, 8).

But, while this adaptive process increases energy production in the short-term to deal with immediate energy deficits, it has the opposite effect over time.

 

Energy Regulation Over Time

As you read earlier, if there’s a lack of available energy over time, our bodies adapt by downregulating energetically expensive functions in order to conserve energy and improve our ability to survive.

This is partially accomplished through the direct effects of the stress hormones, which would be produced in response to the constant energy deficits. Over time, these hormones have direct downregulating effects on many important processes, including metabolic function, immune function, reproductive function, cognitive function, and digestive function (8, 9, 10, 11, 12, 13, 14, 15, 16, 17).

However, this is also accomplished by influencing the higher-level hormones, which regulate our bodies’ functions over time. The most noteworthy of these hormones include the thyroid hormones and the reproductive hormones (which affect a lot more than just reproduction).

These hormones have effects on virtually all bodily processes, including metabolic function (18, 19, 20), immune function (21, 22, 23), reproductive function, cognitive function (24), digestive function (25, 26, 27), and virtually every other aspect of our health (28).

When we experience low energy availability over time, the production of these hormones is reduced, which downregulates all these processes. The reductions in these hormones are largely carried out by the stress hormones, which are elevated during times of low energy availability.

The stress hormones reduce the production of thyroid hormones and the conversion of T4 to T3 (9, 29, 30, 31, 32, 33) while also reducing the production of the reproductive hormones (14, 34).

While this may appear to be detrimental, remember that these adaptive mechanisms allow us to survive in suboptimal environments. We’re extremely energy-demanding organisms, so downregulating our higher-level functions goes a long way for conserving energy and increasing our chances of survival.

But, this certainly isn’t ideal as far as our health is concerned, which is why increasing energy availability is the key to improving our health. When we have high energy availability over time, the production of stress hormones is reduced. This lack of stress hormones signals that energy levels are high, leading to the uninhibited production of thyroid and reproductive hormones and allowing our higher-level functions to continue.

 

Don’t Shoot The Messengers

While hormones are integral parts of our adaptive processes, they aren’t the underlying cause of any dysfunction. Rather, they’re a representation of the conditions of our internal environment and how our bodies are responding to it.

So, they would more accurately be considered a symptom of underlying function, just like high blood sugar or elevated blood pressure. Hormonal imbalance is not the reason someone has PMS, blood sugar dysregulation, thyroid dysfunction, or any other issue, just like high blood sugar isn’t the reason someone has insulin resistance.

The often misplaced focus on hormones as the cause of a particular issue can be extremely problematic, as it directs our attention to a symptom, rather than the true underlying cause. Our focus would be far better placed on the underlying energetic state that leads to the hormonal changes.

So does this mean that hormones don’t matter or that hormones can’t be helpful indicators of our health?

Of course not.

But it does mean that if we want to effectively treat any issue, we must do so on the energetic level by addressing the factors that affect the production and usage of energy.

Improving energy balance is much easier said than done, as this process can be supported and inhibited by various factors. If you’d like more detailed information about how you can improve energy balance, sign up for the free health and energy balance mini-course below, where I outline several of the key factors affecting energy production and usage, how they affect our health, and what you can do about them.

 

References

Hormones: Don’t Shoot The Messengers

Hormones are a common focus when it comes to our health, especially in the alternative field. Hormone imbalances are considered to cause various issues, including hypothyroidism, blood sugar dysregulation, acne, PMS, PCOS, weight gain, mood instability, depression, and many others. As a result, our hormones have become the targets for various interventions.

Foods, supplements, medications, or hormonal replacements are used to “improve our hormonal health” and resolve any of these issues. But, like many other reductionist tendencies, this kind of thinking can lead us astray.

In the same way that our heart doesn’t function independently of our brain or liver or gut, our hormones aren’t a separate, independent feature of our health. In fact, they’re almost exactly the opposite.

Hormones are part of the body’s response to its internal environment. They provide signals based on the environmental conditions, including the availability of energy, which then allows us to best adapt to the circumstances we’re faced with. Because they respond to our internal environment in both the short- and long-term, our hormones are a direct reflection of our general state of health.

In this article, I’m going to shed some light on the adaptive roles of our hormones and how they’re related to our energetic state, while also explaining why interventions aimed at improving hormonal health are often misguided and can distract from the real issues that need to be addressed.

 

Hormones and Energy Balance

In a recent article I explained that energy is the most fundamental force driving our health. It allows every cell in our body to function, and as such is the basic determinant of how well our bodies function.

The amount of energy available to us is dependent on our environment. The amount and type of foods we eat, sunlight exposure, physical and mental activity, and many other factors in our environment determine how much energy our bodies can produce and use.

Our bodies are then designed to adapt to their environment based on the amount of energy available. And this is where the energy-regulating hormones come in.

Our energy-regulating hormones are a major part of this adaptive process. They act as signals that regulate our bodies’ functions based on the amount of energy available.

If there’s a lot of energy available, these hormones will upregulate our energetically expensive functions that allow us to operate optimally. But if there’s not a lot of energy available, these hormones will downregulate these energetically expensive functions in order to conserve energy, kind of like “low-battery mode.”

These changes allow us to survive longer during times of low energy availability and thrive during times of high energy availability.

 

Acute Regulation of Energy Availability

The primary hormones that regulate acute energy availability are glucagon, adrenaline (or epinephrine), and cortisol. These hormones also happen to be the major blood sugar regulating hormones.

This is no accident – as I explained in this article on blood sugar regulation, our blood sugar is one of the most sensitive indicators of our energetic environment as it’s responsible for supplying fuel to our brain and the rest of our bodies.

When energy availability is low, whether it’s due to a lack of fuel (low blood sugar), the inhibition of energy production, or the increased usage of energy, these hormones are released (1). They’re therefore considered to be stress hormones, as they’re produced when the body is under stress due to a lack of energy.

(The categorization of these hormones as “stress hormones” has led to the mistaken idea that these hormones are primarily produced in response to psychological stress, but any stressor can increase the usage of energy, potentially causing the production of these hormones. This includes physical activity such as exercise, as well as mental activity like problem-solving, processing emotions, and what we would consider “psychological stress.”)

In response to this lack of energy, these hormones increase fuel availability by elevating our blood sugar and increasing the production of free fatty acids while also stimulating energy production so that we can deal with the energy deficit at hand (1, 2, 3, 4, 5). They also make us hungry and increase cravings for carbohydrates to increase the availability of fuel (1, 6, 7, 8).

But, while this adaptive process increases energy production in the short-term to deal with immediate energy deficits, it has the opposite effect over time.

 

Energy Regulation Over Time

As you read earlier, if there’s a lack of available energy over time, our bodies adapt by downregulating energetically expensive functions in order to conserve energy and improve our ability to survive.

This is partially accomplished through the direct effects of the stress hormones, which would be produced in response to the constant energy deficits. Over time, these hormones have direct downregulating effects on many important processes, including metabolic function, immune function, reproductive function, cognitive function, and digestive function (8, 9, 10, 11, 12, 13, 14, 15, 16, 17).

However, this is also accomplished by influencing the higher-level hormones, which regulate our bodies’ functions over time. The most noteworthy of these hormones include the thyroid hormones and the reproductive hormones (which affect a lot more than just reproduction).

These hormones have effects on virtually all bodily processes, including metabolic function (18, 19, 20), immune function (21, 22, 23), reproductive function, cognitive function (24), digestive function (25, 26, 27), and virtually every other aspect of our health (28).

When we experience low energy availability over time, the production of these hormones is reduced, which downregulates all these processes. The reductions in these hormones are largely carried out by the stress hormones, which are elevated during times of low energy availability.

The stress hormones reduce the production of thyroid hormones and the conversion of T4 to T3 (9, 29, 30, 31, 32, 33) while also reducing the production of the reproductive hormones (14, 34).

While this may appear to be detrimental, remember that these adaptive mechanisms allow us to survive in suboptimal environments. We’re extremely energy-demanding organisms, so downregulating our higher-level functions goes a long way for conserving energy and increasing our chances of survival.

But, this certainly isn’t ideal as far as our health is concerned, which is why increasing energy availability is the key to improving our health. When we have high energy availability over time, the production of stress hormones is reduced. This lack of stress hormones signals that energy levels are high, leading to the uninhibited production of thyroid and reproductive hormones and allowing our higher-level functions to continue.

 

Don’t Shoot The Messengers

While hormones are integral parts of our adaptive processes, they aren’t the underlying cause of any dysfunction. Rather, they’re a representation of the conditions of our internal environment and how our bodies are responding to it.

So, they would more accurately be considered a symptom of underlying function, just like high blood sugar or elevated blood pressure. Hormonal imbalance is not the reason someone has PMS, blood sugar dysregulation, thyroid dysfunction, or any other issue, just like high blood sugar isn’t the reason someone has insulin resistance.

The often misplaced focus on hormones as the cause of a particular issue can be extremely problematic, as it directs our attention to a symptom, rather than the true underlying cause. Our focus would be far better placed on the underlying energetic state that leads to the hormonal changes.

So does this mean that hormones don’t matter or that hormones can’t be helpful indicators of our health?

Of course not.

But it does mean that if we want to effectively treat any issue, we must do so on the energetic level by addressing the factors that affect the production and usage of energy.

Improving energy balance is much easier said than done, as this process can be supported and inhibited by various factors. If you’d like more detailed information about how you can improve energy balance, sign up for the free health and energy balance mini-course below, where I outline several of the key factors affecting energy production and usage, how they affect our health, and what you can do about them.

 

References

Hormones: Don’t Shoot The Messengers

Hormones are a common focus when it comes to our health, especially in the alternative field. Hormone imbalances are considered to cause various issues, including hypothyroidism, blood sugar dysregulation, acne, PMS, PCOS, weight gain, mood instability, depression, and many others. As a result, our hormones have become the targets for various interventions.

Foods, supplements, medications, or hormonal replacements are used to “improve our hormonal health” and resolve any of these issues. But, like many other reductionist tendencies, this kind of thinking can lead us astray.

In the same way that our heart doesn’t function independently of our brain or liver or gut, our hormones aren’t a separate, independent feature of our health. In fact, they’re almost exactly the opposite.

Hormones are part of the body’s response to its internal environment. They provide signals based on the environmental conditions, including the availability of energy, which then allows us to best adapt to the circumstances we’re faced with. Because they respond to our internal environment in both the short- and long-term, our hormones are a direct reflection of our general state of health.

In this article, I’m going to shed some light on the adaptive roles of our hormones and how they’re related to our energetic state, while also explaining why interventions aimed at improving hormonal health are often misguided and can distract from the real issues that need to be addressed.

 

Hormones and Energy Balance

In a recent article I explained that energy is the most fundamental force driving our health. It allows every cell in our body to function, and as such is the basic determinant of how well our bodies function.

The amount of energy available to us is dependent on our environment. The amount and type of foods we eat, sunlight exposure, physical and mental activity, and many other factors in our environment determine how much energy our bodies can produce and use.

Our bodies are then designed to adapt to their environment based on the amount of energy available. And this is where the energy-regulating hormones come in.

Our energy-regulating hormones are a major part of this adaptive process. They act as signals that regulate our bodies’ functions based on the amount of energy available.

If there’s a lot of energy available, these hormones will upregulate our energetically expensive functions that allow us to operate optimally. But if there’s not a lot of energy available, these hormones will downregulate these energetically expensive functions in order to conserve energy, kind of like “low-battery mode.”

These changes allow us to survive longer during times of low energy availability and thrive during times of high energy availability.

 

Acute Regulation of Energy Availability

The primary hormones that regulate acute energy availability are glucagon, adrenaline (or epinephrine), and cortisol. These hormones also happen to be the major blood sugar regulating hormones.

This is no accident – as I explained in this article on blood sugar regulation, our blood sugar is one of the most sensitive indicators of our energetic environment as it’s responsible for supplying fuel to our brain and the rest of our bodies.

When energy availability is low, whether it’s due to a lack of fuel (low blood sugar), the inhibition of energy production, or the increased usage of energy, these hormones are released (1). They’re therefore considered to be stress hormones, as they’re produced when the body is under stress due to a lack of energy.

(The categorization of these hormones as “stress hormones” has led to the mistaken idea that these hormones are primarily produced in response to psychological stress, but any stressor can increase the usage of energy, potentially causing the production of these hormones. This includes physical activity such as exercise, as well as mental activity like problem-solving, processing emotions, and what we would consider “psychological stress.”)

In response to this lack of energy, these hormones increase fuel availability by elevating our blood sugar and increasing the production of free fatty acids while also stimulating energy production so that we can deal with the energy deficit at hand (1, 2, 3, 4, 5). They also make us hungry and increase cravings for carbohydrates to increase the availability of fuel (1, 6, 7, 8).

But, while this adaptive process increases energy production in the short-term to deal with immediate energy deficits, it has the opposite effect over time.

 

Energy Regulation Over Time

As you read earlier, if there’s a lack of available energy over time, our bodies adapt by downregulating energetically expensive functions in order to conserve energy and improve our ability to survive.

This is partially accomplished through the direct effects of the stress hormones, which would be produced in response to the constant energy deficits. Over time, these hormones have direct downregulating effects on many important processes, including metabolic function, immune function, reproductive function, cognitive function, and digestive function (8, 9, 10, 11, 12, 13, 14, 15, 16, 17).

However, this is also accomplished by influencing the higher-level hormones, which regulate our bodies’ functions over time. The most noteworthy of these hormones include the thyroid hormones and the reproductive hormones (which affect a lot more than just reproduction).

These hormones have effects on virtually all bodily processes, including metabolic function (18, 19, 20), immune function (21, 22, 23), reproductive function, cognitive function (24), digestive function (25, 26, 27), and virtually every other aspect of our health (28).

When we experience low energy availability over time, the production of these hormones is reduced, which downregulates all these processes. The reductions in these hormones are largely carried out by the stress hormones, which are elevated during times of low energy availability.

The stress hormones reduce the production of thyroid hormones and the conversion of T4 to T3 (9, 29, 30, 31, 32, 33) while also reducing the production of the reproductive hormones (14, 34).

While this may appear to be detrimental, remember that these adaptive mechanisms allow us to survive in suboptimal environments. We’re extremely energy-demanding organisms, so downregulating our higher-level functions goes a long way for conserving energy and increasing our chances of survival.

But, this certainly isn’t ideal as far as our health is concerned, which is why increasing energy availability is the key to improving our health. When we have high energy availability over time, the production of stress hormones is reduced. This lack of stress hormones signals that energy levels are high, leading to the uninhibited production of thyroid and reproductive hormones and allowing our higher-level functions to continue.

 

Don’t Shoot The Messengers

While hormones are integral parts of our adaptive processes, they aren’t the underlying cause of any dysfunction. Rather, they’re a representation of the conditions of our internal environment and how our bodies are responding to it.

So, they would more accurately be considered a symptom of underlying function, just like high blood sugar or elevated blood pressure. Hormonal imbalance is not the reason someone has PMS, blood sugar dysregulation, thyroid dysfunction, or any other issue, just like high blood sugar isn’t the reason someone has insulin resistance.

The often misplaced focus on hormones as the cause of a particular issue can be extremely problematic, as it directs our attention to a symptom, rather than the true underlying cause. Our focus would be far better placed on the underlying energetic state that leads to the hormonal changes.

So does this mean that hormones don’t matter or that hormones can’t be helpful indicators of our health?

Of course not.

But it does mean that if we want to effectively treat any issue, we must do so on the energetic level by addressing the factors that affect the production and usage of energy.

Improving energy balance is much easier said than done, as this process can be supported and inhibited by various factors. If you’d like more detailed information about how you can improve energy balance, sign up for the free health and energy balance mini-course below, where I outline several of the key factors affecting energy production and usage, how they affect our health, and what you can do about them.

 

References

Hormones: Don’t Shoot The Messengers

Hormones are a common focus when it comes to our health, especially in the alternative field. Hormone imbalances are considered to cause various issues, including hypothyroidism, blood sugar dysregulation, acne, PMS, PCOS, weight gain, mood instability, depression, and many others. As a result, our hormones have become the targets for various interventions.

Foods, supplements, medications, or hormonal replacements are used to “improve our hormonal health” and resolve any of these issues. But, like many other reductionist tendencies, this kind of thinking can lead us astray.

In the same way that our heart doesn’t function independently of our brain or liver or gut, our hormones aren’t a separate, independent feature of our health. In fact, they’re almost exactly the opposite.

Hormones are part of the body’s response to its internal environment. They provide signals based on the environmental conditions, including the availability of energy, which then allows us to best adapt to the circumstances we’re faced with. Because they respond to our internal environment in both the short- and long-term, our hormones are a direct reflection of our general state of health.

In this article, I’m going to shed some light on the adaptive roles of our hormones and how they’re related to our energetic state, while also explaining why interventions aimed at improving hormonal health are often misguided and can distract from the real issues that need to be addressed.

 

Hormones and Energy Balance

In a recent article I explained that energy is the most fundamental force driving our health. It allows every cell in our body to function, and as such is the basic determinant of how well our bodies function.

The amount of energy available to us is dependent on our environment. The amount and type of foods we eat, sunlight exposure, physical and mental activity, and many other factors in our environment determine how much energy our bodies can produce and use.

Our bodies are then designed to adapt to their environment based on the amount of energy available. And this is where the energy-regulating hormones come in.

Our energy-regulating hormones are a major part of this adaptive process. They act as signals that regulate our bodies’ functions based on the amount of energy available.

If there’s a lot of energy available, these hormones will upregulate our energetically expensive functions that allow us to operate optimally. But if there’s not a lot of energy available, these hormones will downregulate these energetically expensive functions in order to conserve energy, kind of like “low-battery mode.”

These changes allow us to survive longer during times of low energy availability and thrive during times of high energy availability.

 

Acute Regulation of Energy Availability

The primary hormones that regulate acute energy availability are glucagon, adrenaline (or epinephrine), and cortisol. These hormones also happen to be the major blood sugar regulating hormones.

This is no accident – as I explained in this article on blood sugar regulation, our blood sugar is one of the most sensitive indicators of our energetic environment as it’s responsible for supplying fuel to our brain and the rest of our bodies.

When energy availability is low, whether it’s due to a lack of fuel (low blood sugar), the inhibition of energy production, or the increased usage of energy, these hormones are released (1). They’re therefore considered to be stress hormones, as they’re produced when the body is under stress due to a lack of energy.

(The categorization of these hormones as “stress hormones” has led to the mistaken idea that these hormones are primarily produced in response to psychological stress, but any stressor can increase the usage of energy, potentially causing the production of these hormones. This includes physical activity such as exercise, as well as mental activity like problem-solving, processing emotions, and what we would consider “psychological stress.”)

In response to this lack of energy, these hormones increase fuel availability by elevating our blood sugar and increasing the production of free fatty acids while also stimulating energy production so that we can deal with the energy deficit at hand (1, 2, 3, 4, 5). They also make us hungry and increase cravings for carbohydrates to increase the availability of fuel (1, 6, 7, 8).

But, while this adaptive process increases energy production in the short-term to deal with immediate energy deficits, it has the opposite effect over time.

 

Energy Regulation Over Time

As you read earlier, if there’s a lack of available energy over time, our bodies adapt by downregulating energetically expensive functions in order to conserve energy and improve our ability to survive.

This is partially accomplished through the direct effects of the stress hormones, which would be produced in response to the constant energy deficits. Over time, these hormones have direct downregulating effects on many important processes, including metabolic function, immune function, reproductive function, cognitive function, and digestive function (8, 9, 10, 11, 12, 13, 14, 15, 16, 17).

However, this is also accomplished by influencing the higher-level hormones, which regulate our bodies’ functions over time. The most noteworthy of these hormones include the thyroid hormones and the reproductive hormones (which affect a lot more than just reproduction).

These hormones have effects on virtually all bodily processes, including metabolic function (18, 19, 20), immune function (21, 22, 23), reproductive function, cognitive function (24), digestive function (25, 26, 27), and virtually every other aspect of our health (28).

When we experience low energy availability over time, the production of these hormones is reduced, which downregulates all these processes. The reductions in these hormones are largely carried out by the stress hormones, which are elevated during times of low energy availability.

The stress hormones reduce the production of thyroid hormones and the conversion of T4 to T3 (9, 29, 30, 31, 32, 33) while also reducing the production of the reproductive hormones (14, 34).

While this may appear to be detrimental, remember that these adaptive mechanisms allow us to survive in suboptimal environments. We’re extremely energy-demanding organisms, so downregulating our higher-level functions goes a long way for conserving energy and increasing our chances of survival.

But, this certainly isn’t ideal as far as our health is concerned, which is why increasing energy availability is the key to improving our health. When we have high energy availability over time, the production of stress hormones is reduced. This lack of stress hormones signals that energy levels are high, leading to the uninhibited production of thyroid and reproductive hormones and allowing our higher-level functions to continue.

 

Don’t Shoot The Messengers

While hormones are integral parts of our adaptive processes, they aren’t the underlying cause of any dysfunction. Rather, they’re a representation of the conditions of our internal environment and how our bodies are responding to it.

So, they would more accurately be considered a symptom of underlying function, just like high blood sugar or elevated blood pressure. Hormonal imbalance is not the reason someone has PMS, blood sugar dysregulation, thyroid dysfunction, or any other issue, just like high blood sugar isn’t the reason someone has insulin resistance.

The often misplaced focus on hormones as the cause of a particular issue can be extremely problematic, as it directs our attention to a symptom, rather than the true underlying cause. Our focus would be far better placed on the underlying energetic state that leads to the hormonal changes.

So does this mean that hormones don’t matter or that hormones can’t be helpful indicators of our health?

Of course not.

But it does mean that if we want to effectively treat any issue, we must do so on the energetic level by addressing the factors that affect the production and usage of energy.

Improving energy balance is much easier said than done, as this process can be supported and inhibited by various factors. If you’d like more detailed information about how you can improve energy balance, sign up for the free health and energy balance mini-course below, where I outline several of the key factors affecting energy production and usage, how they affect our health, and what you can do about them.

 

References

Hormones: Don’t Shoot The Messengers

Hormones are a common focus when it comes to our health, especially in the alternative field. Hormone imbalances are considered to cause various issues, including hypothyroidism, blood sugar dysregulation, acne, PMS, PCOS, weight gain, mood instability, depression, and many others. As a result, our hormones have become the targets for various interventions.

Foods, supplements, medications, or hormonal replacements are used to “improve our hormonal health” and resolve any of these issues. But, like many other reductionist tendencies, this kind of thinking can lead us astray.

In the same way that our heart doesn’t function independently of our brain or liver or gut, our hormones aren’t a separate, independent feature of our health. In fact, they’re almost exactly the opposite.

Hormones are part of the body’s response to its internal environment. They provide signals based on the environmental conditions, including the availability of energy, which then allows us to best adapt to the circumstances we’re faced with. Because they respond to our internal environment in both the short- and long-term, our hormones are a direct reflection of our general state of health.

In this article, I’m going to shed some light on the adaptive roles of our hormones and how they’re related to our energetic state, while also explaining why interventions aimed at improving hormonal health are often misguided and can distract from the real issues that need to be addressed.

 

Hormones and Energy Balance

In a recent article I explained that energy is the most fundamental force driving our health. It allows every cell in our body to function, and as such is the basic determinant of how well our bodies function.

The amount of energy available to us is dependent on our environment. The amount and type of foods we eat, sunlight exposure, physical and mental activity, and many other factors in our environment determine how much energy our bodies can produce and use.

Our bodies are then designed to adapt to their environment based on the amount of energy available. And this is where the energy-regulating hormones come in.

Our energy-regulating hormones are a major part of this adaptive process. They act as signals that regulate our bodies’ functions based on the amount of energy available.

If there’s a lot of energy available, these hormones will upregulate our energetically expensive functions that allow us to operate optimally. But if there’s not a lot of energy available, these hormones will downregulate these energetically expensive functions in order to conserve energy, kind of like “low-battery mode.”

These changes allow us to survive longer during times of low energy availability and thrive during times of high energy availability.

 

Acute Regulation of Energy Availability

The primary hormones that regulate acute energy availability are glucagon, adrenaline (or epinephrine), and cortisol. These hormones also happen to be the major blood sugar regulating hormones.

This is no accident – as I explained in this article on blood sugar regulation, our blood sugar is one of the most sensitive indicators of our energetic environment as it’s responsible for supplying fuel to our brain and the rest of our bodies.

When energy availability is low, whether it’s due to a lack of fuel (low blood sugar), the inhibition of energy production, or the increased usage of energy, these hormones are released (1). They’re therefore considered to be stress hormones, as they’re produced when the body is under stress due to a lack of energy.

(The categorization of these hormones as “stress hormones” has led to the mistaken idea that these hormones are primarily produced in response to psychological stress, but any stressor can increase the usage of energy, potentially causing the production of these hormones. This includes physical activity such as exercise, as well as mental activity like problem-solving, processing emotions, and what we would consider “psychological stress.”)

In response to this lack of energy, these hormones increase fuel availability by elevating our blood sugar and increasing the production of free fatty acids while also stimulating energy production so that we can deal with the energy deficit at hand (1, 2, 3, 4, 5). They also make us hungry and increase cravings for carbohydrates to increase the availability of fuel (1, 6, 7, 8).

But, while this adaptive process increases energy production in the short-term to deal with immediate energy deficits, it has the opposite effect over time.

 

Energy Regulation Over Time

As you read earlier, if there’s a lack of available energy over time, our bodies adapt by downregulating energetically expensive functions in order to conserve energy and improve our ability to survive.

This is partially accomplished through the direct effects of the stress hormones, which would be produced in response to the constant energy deficits. Over time, these hormones have direct downregulating effects on many important processes, including metabolic function, immune function, reproductive function, cognitive function, and digestive function (8, 9, 10, 11, 12, 13, 14, 15, 16, 17).

However, this is also accomplished by influencing the higher-level hormones, which regulate our bodies’ functions over time. The most noteworthy of these hormones include the thyroid hormones and the reproductive hormones (which affect a lot more than just reproduction).

These hormones have effects on virtually all bodily processes, including metabolic function (18, 19, 20), immune function (21, 22, 23), reproductive function, cognitive function (24), digestive function (25, 26, 27), and virtually every other aspect of our health (28).

When we experience low energy availability over time, the production of these hormones is reduced, which downregulates all these processes. The reductions in these hormones are largely carried out by the stress hormones, which are elevated during times of low energy availability.

The stress hormones reduce the production of thyroid hormones and the conversion of T4 to T3 (9, 29, 30, 31, 32, 33) while also reducing the production of the reproductive hormones (14, 34).

While this may appear to be detrimental, remember that these adaptive mechanisms allow us to survive in suboptimal environments. We’re extremely energy-demanding organisms, so downregulating our higher-level functions goes a long way for conserving energy and increasing our chances of survival.

But, this certainly isn’t ideal as far as our health is concerned, which is why increasing energy availability is the key to improving our health. When we have high energy availability over time, the production of stress hormones is reduced. This lack of stress hormones signals that energy levels are high, leading to the uninhibited production of thyroid and reproductive hormones and allowing our higher-level functions to continue.

 

Don’t Shoot The Messengers

While hormones are integral parts of our adaptive processes, they aren’t the underlying cause of any dysfunction. Rather, they’re a representation of the conditions of our internal environment and how our bodies are responding to it.

So, they would more accurately be considered a symptom of underlying function, just like high blood sugar or elevated blood pressure. Hormonal imbalance is not the reason someone has PMS, blood sugar dysregulation, thyroid dysfunction, or any other issue, just like high blood sugar isn’t the reason someone has insulin resistance.

The often misplaced focus on hormones as the cause of a particular issue can be extremely problematic, as it directs our attention to a symptom, rather than the true underlying cause. Our focus would be far better placed on the underlying energetic state that leads to the hormonal changes.

So does this mean that hormones don’t matter or that hormones can’t be helpful indicators of our health?

Of course not.

But it does mean that if we want to effectively treat any issue, we must do so on the energetic level by addressing the factors that affect the production and usage of energy.

Improving energy balance is much easier said than done, as this process can be supported and inhibited by various factors. If you’d like more detailed information about how you can improve energy balance, sign up for the free health and energy balance mini-course below, where I outline several of the key factors affecting energy production and usage, how they affect our health, and what you can do about them.

 

References

Hormones: Don’t Shoot The Messengers

Hormones are a common focus when it comes to our health, especially in the alternative field. Hormone imbalances are considered to cause various issues, including hypothyroidism, blood sugar dysregulation, acne, PMS, PCOS, weight gain, mood instability, depression, and many others. As a result, our hormones have become the targets for various interventions.

Foods, supplements, medications, or hormonal replacements are used to “improve our hormonal health” and resolve any of these issues. But, like many other reductionist tendencies, this kind of thinking can lead us astray.

In the same way that our heart doesn’t function independently of our brain or liver or gut, our hormones aren’t a separate, independent feature of our health. In fact, they’re almost exactly the opposite.

Hormones are part of the body’s response to its internal environment. They provide signals based on the environmental conditions, including the availability of energy, which then allows us to best adapt to the circumstances we’re faced with. Because they respond to our internal environment in both the short- and long-term, our hormones are a direct reflection of our general state of health.

In this article, I’m going to shed some light on the adaptive roles of our hormones and how they’re related to our energetic state, while also explaining why interventions aimed at improving hormonal health are often misguided and can distract from the real issues that need to be addressed.

 

Hormones and Energy Balance

In a recent article I explained that energy is the most fundamental force driving our health. It allows every cell in our body to function, and as such is the basic determinant of how well our bodies function.

The amount of energy available to us is dependent on our environment. The amount and type of foods we eat, sunlight exposure, physical and mental activity, and many other factors in our environment determine how much energy our bodies can produce and use.

Our bodies are then designed to adapt to their environment based on the amount of energy available. And this is where the energy-regulating hormones come in.

Our energy-regulating hormones are a major part of this adaptive process. They act as signals that regulate our bodies’ functions based on the amount of energy available.

If there’s a lot of energy available, these hormones will upregulate our energetically expensive functions that allow us to operate optimally. But if there’s not a lot of energy available, these hormones will downregulate these energetically expensive functions in order to conserve energy, kind of like “low-battery mode.”

These changes allow us to survive longer during times of low energy availability and thrive during times of high energy availability.

 

Acute Regulation of Energy Availability

The primary hormones that regulate acute energy availability are glucagon, adrenaline (or epinephrine), and cortisol. These hormones also happen to be the major blood sugar regulating hormones.

This is no accident – as I explained in this article on blood sugar regulation, our blood sugar is one of the most sensitive indicators of our energetic environment as it’s responsible for supplying fuel to our brain and the rest of our bodies.

When energy availability is low, whether it’s due to a lack of fuel (low blood sugar), the inhibition of energy production, or the increased usage of energy, these hormones are released (1). They’re therefore considered to be stress hormones, as they’re produced when the body is under stress due to a lack of energy.

(The categorization of these hormones as “stress hormones” has led to the mistaken idea that these hormones are primarily produced in response to psychological stress, but any stressor can increase the usage of energy, potentially causing the production of these hormones. This includes physical activity such as exercise, as well as mental activity like problem-solving, processing emotions, and what we would consider “psychological stress.”)

In response to this lack of energy, these hormones increase fuel availability by elevating our blood sugar and increasing the production of free fatty acids while also stimulating energy production so that we can deal with the energy deficit at hand (1, 2, 3, 4, 5). They also make us hungry and increase cravings for carbohydrates to increase the availability of fuel (1, 6, 7, 8).

But, while this adaptive process increases energy production in the short-term to deal with immediate energy deficits, it has the opposite effect over time.

 

Energy Regulation Over Time

As you read earlier, if there’s a lack of available energy over time, our bodies adapt by downregulating energetically expensive functions in order to conserve energy and improve our ability to survive.

This is partially accomplished through the direct effects of the stress hormones, which would be produced in response to the constant energy deficits. Over time, these hormones have direct downregulating effects on many important processes, including metabolic function, immune function, reproductive function, cognitive function, and digestive function (8, 9, 10, 11, 12, 13, 14, 15, 16, 17).

However, this is also accomplished by influencing the higher-level hormones, which regulate our bodies’ functions over time. The most noteworthy of these hormones include the thyroid hormones and the reproductive hormones (which affect a lot more than just reproduction).

These hormones have effects on virtually all bodily processes, including metabolic function (18, 19, 20), immune function (21, 22, 23), reproductive function, cognitive function (24), digestive function (25, 26, 27), and virtually every other aspect of our health (28).

When we experience low energy availability over time, the production of these hormones is reduced, which downregulates all these processes. The reductions in these hormones are largely carried out by the stress hormones, which are elevated during times of low energy availability.

The stress hormones reduce the production of thyroid hormones and the conversion of T4 to T3 (9, 29, 30, 31, 32, 33) while also reducing the production of the reproductive hormones (14, 34).

While this may appear to be detrimental, remember that these adaptive mechanisms allow us to survive in suboptimal environments. We’re extremely energy-demanding organisms, so downregulating our higher-level functions goes a long way for conserving energy and increasing our chances of survival.

But, this certainly isn’t ideal as far as our health is concerned, which is why increasing energy availability is the key to improving our health. When we have high energy availability over time, the production of stress hormones is reduced. This lack of stress hormones signals that energy levels are high, leading to the uninhibited production of thyroid and reproductive hormones and allowing our higher-level functions to continue.

 

Don’t Shoot The Messengers

While hormones are integral parts of our adaptive processes, they aren’t the underlying cause of any dysfunction. Rather, they’re a representation of the conditions of our internal environment and how our bodies are responding to it.

So, they would more accurately be considered a symptom of underlying function, just like high blood sugar or elevated blood pressure. Hormonal imbalance is not the reason someone has PMS, blood sugar dysregulation, thyroid dysfunction, or any other issue, just like high blood sugar isn’t the reason someone has insulin resistance.

The often misplaced focus on hormones as the cause of a particular issue can be extremely problematic, as it directs our attention to a symptom, rather than the true underlying cause. Our focus would be far better placed on the underlying energetic state that leads to the hormonal changes.

So does this mean that hormones don’t matter or that hormones can’t be helpful indicators of our health?

Of course not.

But it does mean that if we want to effectively treat any issue, we must do so on the energetic level by addressing the factors that affect the production and usage of energy.

Improving energy balance is much easier said than done, as this process can be supported and inhibited by various factors. If you’d like more detailed information about how you can improve energy balance, sign up for the free health and energy balance mini-course below, where I outline several of the key factors affecting energy production and usage, how they affect our health, and what you can do about them.

 

References

Water: More is NOT Better

The recommendation to drink more water is probably the most common and universally agreed upon advice given in the health industry, maybe second only to the suggestion to avoid sugar.

Most everybody has heard that they should start their day with a big glass of water and drink 8 glasses of water a day, and others even suggest that this isn’t enough. Some recommend drinking as much as ½ or even 1 oz of water per pound of bodyweight (this would be 18 glasses of water per day for someone weighing 150 lbs.)

And why wouldn’t we drink that much water?

Water is the essence of life. It has no calories and makes up as much as 60% of our body weight. Plus, it keeps us full so we eat less while also keeping our skin moisturized, wrinkle-free, and glowing. Oh, and did I mention it increases our metabolism too?

Better get chugging…

Yes, that was sarcasm. But it’s allowed because I believed all those things at one point too. For years I was known for never being seen without a water bottle and for getting multiple water refills whenever I was out to eat. I was always drinking water.

But, the dogmatic belief that drinking more water is better for our health is almost entirely unfounded, and most of the research actually points in the opposite direction.

 

The “Benefits” of Drinking More Water

It’s important to first acknowledge that water is not benign. While those that recommend drinking more water often recognize the dangers of dehydration, they ignore the dangers of overhydration. Overhydration can cause many of the same effects as dehydration, including headaches, impaired cognitive function, and even death.

I’ll explain exactly why overhydration is so dangerous in a little bit, but let’s first break down the supposed benefits of drinking water.

First is that water keeps us fuller, causing us to eat less, and has no calories, making it a healthy replacement for beverages that do contain calories. And this is at least somewhat true – drinking more water can make us eat slightly less (1, 2, 3).

But, as you may have read in several of my previous articles, eating less is NOT the answer for fat loss or improved health, and instead leads to stress and degeneration. And, the idea that having calories makes something less healthy is based on the heavily flawed calories-in/calories-out equation, which I described in this article.

The second supposed benefit is that water “increases our metabolism.” Again, this isn’t entirely untrue, as drinking water has been shown to increase energy expenditure by a small amount (around 24 calories per 500 mL) (4). But, this doesn’t mean that it improves metabolic function, will lead to fat loss, or that it’s even beneficial at all. In fact, this increase in energy expenditure is a sign of stress, which I’ll explain further in a little bit.

Third is the assumption that drinking more water increases hydration. Much of the advice to drink more water is based on the idea that dehydration is bad, so drinking water must be good. But, while dehydration is a legitimate issue (although not a very common one), simply drinking lots of water isn’t the best way to solve it.

In order for our cells to use water, they require minerals like sodium, potassium, and magnesium, as well as energy. Water is typically devoid of all those things, so drinking water won’t necessarily increase hydration and can even reduce cellular hydration because it lacks those other important nutrients.

Water is purported to have many other benefits, like relieving headaches and constipation. However, drinking water only helps these symptoms if dehydration was the cause of these symptoms, which often isn’t the case (5, 6). And, if these symptoms weren’t caused by dehydration, drinking water can make them even worse.

Other supposed benefits of drinking lots of water, like “flushing out toxins” and “boosting our immune system,” are mostly fabricated ideas that are, at best, based on a heavily flawed understanding of these features of physiology.

 

Water and Stress

There’s one major problem that comes with drinking lots of water. It’s actually the same issue that causes the extreme effects of overhydration, like headaches, impaired cognitive function, and death, although on a smaller scale.

And that problem is that it dilutes our blood, which reduces the concentration of various electrolytes, most importantly sodium.

The sodium level in our blood is tightly regulated. And, when it drops too low, our body’s stress systems are activated (7, 8). This leads to the production of stress hormones like aldosterone, which cause our bodies to retain more sodium (and excrete less) in order to increase the sodium concentration.

But, retaining sodium comes at a cost – the sodium we would normally excrete in our kidneys is replaced with potassium and magnesium, leading to the loss of greater amounts of these minerals (9).

A lack of potassium and magnesium, as well as the stress hormones themselves, then leads to cell swelling (10, 11, 12, 13). This swelling inhibits our ability to produce and use energy, which is disastrous for every aspect of our health (14).

I explain the cascade of events involved in this adaptive process more thoroughly in this article on salt consumption, but to summarize, a lowered sodium concentration in the blood (either due to drinking too much water or consuming too little sodium), can be extremely stressful on our bodies and has many negative consequences.

And, this is seen quite clearly in the research showing that drinking water increases energy expenditure (these are the studies often cited for water’s ability to “increase our metabolism”).

These studies have shown that this increase in energy expenditure is directly caused by the stress that results from a lowered sodium concentration in the blood (15, 16). This finding has been corroborated by several studies showing that drinking plain water leads to stress but drinking water with enough salt to mimic our normal blood sodium concentrations doesn’t (16, 17, 18, 19).

In other words, forcing ourselves to drink excess water can lead to stress and cell swelling, which negatively affects metabolic function.

But, as I’ll explain in a second, while drinking too much water can be harmful, we don’t have to worry much about it if we simply listen to our body’s innate signals that tell us how much we need to drink.

 

Thirst Has Got You Covered

The moral of the story is that more water is not better. So, there’s no need to force ourselves to drink a certain amount of water each day, which can be far more harmful than helpful. Instead, our bodies have their own hydration sensors that tell us when and how much we need to drink, so we can simply drink when we’re thirsty!

There’s a common myth that by the time you’re feeling thirsty you’re already dehydrated, but this is simply unsupported, as is explained in this quote:

“It is often stated in the lay press (17, 19, 22, 26) and even in professional journals (47) that by the time a person is thirsty that person is already dehydrated. In a number of scientific treatises on thirst, one finds no such assertion (1, 12, 30, 67, 69, 76, 98). On the contrary, a rise in plasma osmolality of less than 2% can elicit thirst, whereas most experts would define dehydration as beginning when a person has lost 3% or more of body weight (96), which translates into a rise in plasma osmolality of at least 5%.” (20)

And, as stated in these quotes, our sense of thirst is extremely sensitive, and it wouldn’t make sense biologically if we had to force ourselves to drink more water than we naturally wanted to just to remain hydrated:

“To prevent dehydration reptiles, birds, vertebrates, and all land animals have evolved an exquisitely sensitive network of physiological controls to maintain body water and fluid intake by thirst.” (6)

“Osmotic regulation of vasopressin secretion and thirst is so sensitive, quick, and accurate (67) that it is hard to imagine that evolutionary development left us with a chronic water deficit that has to be compensated by forcing fluid intake.” (20)

[Note: there’s also a common myth that if your pee isn’t clear you’re dehydrated, but this simply isn’t true (20).]

So, it’s quite clear that by using our sense of thirst, our body’s built-in hydration indicator, we can remain adequately hydrated.

 

Why Water?

There’s no need to limit our beverages to only water. There are tons of other options that come with added nutrients and taste better.

Fruit juice, milk, and tea or coffee with honey or sugar are all great options. These options have nutrients that allow us to produce energy and minerals needed for effective hydration, which water doesn’t have. (If you’re worried about the sugar in these drinks, check out these articles.)

Of course, this doesn’t mean that we need to avoid water, just that other drinks can be even better. And, if we’re drinking more water because we’re sweating a lot or for some other reason, it’s important to make sure we’re also getting enough sodium and other minerals to effectively rehydrate.

 

Just to hammer the point home, forcing ourselves to drink more water is not beneficial for our health, as is commonly suggested. Rather, we can rely on our sense of thirst to keep us hydrated, and we can also choose drinks other than water that contain the nutrients we need to produce energy and keep our cells hydrated.

 

References

Water: More is NOT Better

The recommendation to drink more water is probably the most common and universally agreed upon advice given in the health industry, maybe second only to the suggestion to avoid sugar.

Most everybody has heard that they should start their day with a big glass of water and drink 8 glasses of water a day, and others even suggest that this isn’t enough. Some recommend drinking as much as ½ or even 1 oz of water per pound of bodyweight (this would be 18 glasses of water per day for someone weighing 150 lbs.)

And why wouldn’t we drink that much water?

Water is the essence of life. It has no calories and makes up as much as 60% of our body weight. Plus, it keeps us full so we eat less while also keeping our skin moisturized, wrinkle-free, and glowing. Oh, and did I mention it increases our metabolism too?

Better get chugging…

Yes, that was sarcasm. But it’s allowed because I believed all those things at one point too. For years I was known for never being seen without a water bottle and for getting multiple water refills whenever I was out to eat. I was always drinking water.

But, the dogmatic belief that drinking more water is better for our health is almost entirely unfounded, and most of the research actually points in the opposite direction.

 

The “Benefits” of Drinking More Water

It’s important to first acknowledge that water is not benign. While those that recommend drinking more water often recognize the dangers of dehydration, they ignore the dangers of overhydration. Overhydration can cause many of the same effects as dehydration, including headaches, impaired cognitive function, and even death.

I’ll explain exactly why overhydration is so dangerous in a little bit, but let’s first break down the supposed benefits of drinking water.

First is that water keeps us fuller, causing us to eat less, and has no calories, making it a healthy replacement for beverages that do contain calories. And this is at least somewhat true – drinking more water can make us eat slightly less (1, 2, 3).

But, as you may have read in several of my previous articles, eating less is NOT the answer for fat loss or improved health, and instead leads to stress and degeneration. And, the idea that having calories makes something less healthy is based on the heavily flawed calories-in/calories-out equation, which I described in this article.

The second supposed benefit is that water “increases our metabolism.” Again, this isn’t entirely untrue, as drinking water has been shown to increase energy expenditure by a small amount (around 24 calories per 500 mL) (4). But, this doesn’t mean that it improves metabolic function, will lead to fat loss, or that it’s even beneficial at all. In fact, this increase in energy expenditure is a sign of stress, which I’ll explain further in a little bit.

Third is the assumption that drinking more water increases hydration. Much of the advice to drink more water is based on the idea that dehydration is bad, so drinking water must be good. But, while dehydration is a legitimate issue (although not a very common one), simply drinking lots of water isn’t the best way to solve it.

In order for our cells to use water, they require minerals like sodium, potassium, and magnesium, as well as energy. Water is typically devoid of all those things, so drinking water won’t necessarily increase hydration and can even reduce cellular hydration because it lacks those other important nutrients.

Water is purported to have many other benefits, like relieving headaches and constipation. However, drinking water only helps these symptoms if dehydration was the cause of these symptoms, which often isn’t the case (5, 6). And, if these symptoms weren’t caused by dehydration, drinking water can make them even worse.

Other supposed benefits of drinking lots of water, like “flushing out toxins” and “boosting our immune system,” are mostly fabricated ideas that are, at best, based on a heavily flawed understanding of these features of physiology.

 

Water and Stress

There’s one major problem that comes with drinking lots of water. It’s actually the same issue that causes the extreme effects of overhydration, like headaches, impaired cognitive function, and death, although on a smaller scale.

And that problem is that it dilutes our blood, which reduces the concentration of various electrolytes, most importantly sodium.

The sodium level in our blood is tightly regulated. And, when it drops too low, our body’s stress systems are activated (7, 8). This leads to the production of stress hormones like aldosterone, which cause our bodies to retain more sodium (and excrete less) in order to increase the sodium concentration.

But, retaining sodium comes at a cost – the sodium we would normally excrete in our kidneys is replaced with potassium and magnesium, leading to the loss of greater amounts of these minerals (9).

A lack of potassium and magnesium, as well as the stress hormones themselves, then leads to cell swelling (10, 11, 12, 13). This swelling inhibits our ability to produce and use energy, which is disastrous for every aspect of our health (14).

I explain the cascade of events involved in this adaptive process more thoroughly in this article on salt consumption, but to summarize, a lowered sodium concentration in the blood (either due to drinking too much water or consuming too little sodium), can be extremely stressful on our bodies and has many negative consequences.

And, this is seen quite clearly in the research showing that drinking water increases energy expenditure (these are the studies often cited for water’s ability to “increase our metabolism”).

These studies have shown that this increase in energy expenditure is directly caused by the stress that results from a lowered sodium concentration in the blood (15, 16). This finding has been corroborated by several studies showing that drinking plain water leads to stress but drinking water with enough salt to mimic our normal blood sodium concentrations doesn’t (16, 17, 18, 19).

In other words, forcing ourselves to drink excess water can lead to stress and cell swelling, which negatively affects metabolic function.

But, as I’ll explain in a second, while drinking too much water can be harmful, we don’t have to worry much about it if we simply listen to our body’s innate signals that tell us how much we need to drink.

 

Thirst Has Got You Covered

The moral of the story is that more water is not better. So, there’s no need to force ourselves to drink a certain amount of water each day, which can be far more harmful than helpful. Instead, our bodies have their own hydration sensors that tell us when and how much we need to drink, so we can simply drink when we’re thirsty!

There’s a common myth that by the time you’re feeling thirsty you’re already dehydrated, but this is simply unsupported, as is explained in this quote:

“It is often stated in the lay press (17, 19, 22, 26) and even in professional journals (47) that by the time a person is thirsty that person is already dehydrated. In a number of scientific treatises on thirst, one finds no such assertion (1, 12, 30, 67, 69, 76, 98). On the contrary, a rise in plasma osmolality of less than 2% can elicit thirst, whereas most experts would define dehydration as beginning when a person has lost 3% or more of body weight (96), which translates into a rise in plasma osmolality of at least 5%.” (20)

And, as stated in these quotes, our sense of thirst is extremely sensitive, and it wouldn’t make sense biologically if we had to force ourselves to drink more water than we naturally wanted to just to remain hydrated:

“To prevent dehydration reptiles, birds, vertebrates, and all land animals have evolved an exquisitely sensitive network of physiological controls to maintain body water and fluid intake by thirst.” (6)

“Osmotic regulation of vasopressin secretion and thirst is so sensitive, quick, and accurate (67) that it is hard to imagine that evolutionary development left us with a chronic water deficit that has to be compensated by forcing fluid intake.” (20)

[Note: there’s also a common myth that if your pee isn’t clear you’re dehydrated, but this simply isn’t true (20).]

So, it’s quite clear that by using our sense of thirst, our body’s built-in hydration indicator, we can remain adequately hydrated.

 

Why Water?

There’s no need to limit our beverages to only water. There are tons of other options that come with added nutrients and taste better.

Fruit juice, milk, and tea or coffee with honey or sugar are all great options. These options have nutrients that allow us to produce energy and minerals needed for effective hydration, which water doesn’t have. (If you’re worried about the sugar in these drinks, check out these articles.)

Of course, this doesn’t mean that we need to avoid water, just that other drinks can be even better. And, if we’re drinking more water because we’re sweating a lot or for some other reason, it’s important to make sure we’re also getting enough sodium and other minerals to effectively rehydrate.

 

Just to hammer the point home, forcing ourselves to drink more water is not beneficial for our health, as is commonly suggested. Rather, we can rely on our sense of thirst to keep us hydrated, and we can also choose drinks other than water that contain the nutrients we need to produce energy and keep our cells hydrated.

 

References

Water: More is NOT Better

The recommendation to drink more water is probably the most common and universally agreed upon advice given in the health industry, maybe second only to the suggestion to avoid sugar.

Most everybody has heard that they should start their day with a big glass of water and drink 8 glasses of water a day, and others even suggest that this isn’t enough. Some recommend drinking as much as ½ or even 1 oz of water per pound of bodyweight (this would be 18 glasses of water per day for someone weighing 150 lbs.)

And why wouldn’t we drink that much water?

Water is the essence of life. It has no calories and makes up as much as 60% of our body weight. Plus, it keeps us full so we eat less while also keeping our skin moisturized, wrinkle-free, and glowing. Oh, and did I mention it increases our metabolism too?

Better get chugging…

Yes, that was sarcasm. But it’s allowed because I believed all those things at one point too. For years I was known for never being seen without a water bottle and for getting multiple water refills whenever I was out to eat. I was always drinking water.

But, the dogmatic belief that drinking more water is better for our health is almost entirely unfounded, and most of the research actually points in the opposite direction.

 

The “Benefits” of Drinking More Water

It’s important to first acknowledge that water is not benign. While those that recommend drinking more water often recognize the dangers of dehydration, they ignore the dangers of overhydration. Overhydration can cause many of the same effects as dehydration, including headaches, impaired cognitive function, and even death.

I’ll explain exactly why overhydration is so dangerous in a little bit, but let’s first break down the supposed benefits of drinking water.

First is that water keeps us fuller, causing us to eat less, and has no calories, making it a healthy replacement for beverages that do contain calories. And this is at least somewhat true – drinking more water can make us eat slightly less (1, 2, 3).

But, as you may have read in several of my previous articles, eating less is NOT the answer for fat loss or improved health, and instead leads to stress and degeneration. And, the idea that having calories makes something less healthy is based on the heavily flawed calories-in/calories-out equation, which I described in this article.

The second supposed benefit is that water “increases our metabolism.” Again, this isn’t entirely untrue, as drinking water has been shown to increase energy expenditure by a small amount (around 24 calories per 500 mL) (4). But, this doesn’t mean that it improves metabolic function, will lead to fat loss, or that it’s even beneficial at all. In fact, this increase in energy expenditure is a sign of stress, which I’ll explain further in a little bit.

Third is the assumption that drinking more water increases hydration. Much of the advice to drink more water is based on the idea that dehydration is bad, so drinking water must be good. But, while dehydration is a legitimate issue (although not a very common one), simply drinking lots of water isn’t the best way to solve it.

In order for our cells to use water, they require minerals like sodium, potassium, and magnesium, as well as energy. Water is typically devoid of all those things, so drinking water won’t necessarily increase hydration and can even reduce cellular hydration because it lacks those other important nutrients.

Water is purported to have many other benefits, like relieving headaches and constipation. However, drinking water only helps these symptoms if dehydration was the cause of these symptoms, which often isn’t the case (5, 6). And, if these symptoms weren’t caused by dehydration, drinking water can make them even worse.

Other supposed benefits of drinking lots of water, like “flushing out toxins” and “boosting our immune system,” are mostly fabricated ideas that are, at best, based on a heavily flawed understanding of these features of physiology.

 

Water and Stress

There’s one major problem that comes with drinking lots of water. It’s actually the same issue that causes the extreme effects of overhydration, like headaches, impaired cognitive function, and death, although on a smaller scale.

And that problem is that it dilutes our blood, which reduces the concentration of various electrolytes, most importantly sodium.

The sodium level in our blood is tightly regulated. And, when it drops too low, our body’s stress systems are activated (7, 8). This leads to the production of stress hormones like aldosterone, which cause our bodies to retain more sodium (and excrete less) in order to increase the sodium concentration.

But, retaining sodium comes at a cost – the sodium we would normally excrete in our kidneys is replaced with potassium and magnesium, leading to the loss of greater amounts of these minerals (9).

A lack of potassium and magnesium, as well as the stress hormones themselves, then leads to cell swelling (10, 11, 12, 13). This swelling inhibits our ability to produce and use energy, which is disastrous for every aspect of our health (14).

I explain the cascade of events involved in this adaptive process more thoroughly in this article on salt consumption, but to summarize, a lowered sodium concentration in the blood (either due to drinking too much water or consuming too little sodium), can be extremely stressful on our bodies and has many negative consequences.

And, this is seen quite clearly in the research showing that drinking water increases energy expenditure (these are the studies often cited for water’s ability to “increase our metabolism”).

These studies have shown that this increase in energy expenditure is directly caused by the stress that results from a lowered sodium concentration in the blood (15, 16). This finding has been corroborated by several studies showing that drinking plain water leads to stress but drinking water with enough salt to mimic our normal blood sodium concentrations doesn’t (16, 17, 18, 19).

In other words, forcing ourselves to drink excess water can lead to stress and cell swelling, which negatively affects metabolic function.

But, as I’ll explain in a second, while drinking too much water can be harmful, we don’t have to worry much about it if we simply listen to our body’s innate signals that tell us how much we need to drink.

 

Thirst Has Got You Covered

The moral of the story is that more water is not better. So, there’s no need to force ourselves to drink a certain amount of water each day, which can be far more harmful than helpful. Instead, our bodies have their own hydration sensors that tell us when and how much we need to drink, so we can simply drink when we’re thirsty!

There’s a common myth that by the time you’re feeling thirsty you’re already dehydrated, but this is simply unsupported, as is explained in this quote:

“It is often stated in the lay press (17, 19, 22, 26) and even in professional journals (47) that by the time a person is thirsty that person is already dehydrated. In a number of scientific treatises on thirst, one finds no such assertion (1, 12, 30, 67, 69, 76, 98). On the contrary, a rise in plasma osmolality of less than 2% can elicit thirst, whereas most experts would define dehydration as beginning when a person has lost 3% or more of body weight (96), which translates into a rise in plasma osmolality of at least 5%.” (20)

And, as stated in these quotes, our sense of thirst is extremely sensitive, and it wouldn’t make sense biologically if we had to force ourselves to drink more water than we naturally wanted to just to remain hydrated:

“To prevent dehydration reptiles, birds, vertebrates, and all land animals have evolved an exquisitely sensitive network of physiological controls to maintain body water and fluid intake by thirst.” (6)

“Osmotic regulation of vasopressin secretion and thirst is so sensitive, quick, and accurate (67) that it is hard to imagine that evolutionary development left us with a chronic water deficit that has to be compensated by forcing fluid intake.” (20)

[Note: there’s also a common myth that if your pee isn’t clear you’re dehydrated, but this simply isn’t true (20).]

So, it’s quite clear that by using our sense of thirst, our body’s built-in hydration indicator, we can remain adequately hydrated.

 

Why Water?

There’s no need to limit our beverages to only water. There are tons of other options that come with added nutrients and taste better.

Fruit juice, milk, and tea or coffee with honey or sugar are all great options. These options have nutrients that allow us to produce energy and minerals needed for effective hydration, which water doesn’t have. (If you’re worried about the sugar in these drinks, check out these articles.)

Of course, this doesn’t mean that we need to avoid water, just that other drinks can be even better. And, if we’re drinking more water because we’re sweating a lot or for some other reason, it’s important to make sure we’re also getting enough sodium and other minerals to effectively rehydrate.

 

Just to hammer the point home, forcing ourselves to drink more water is not beneficial for our health, as is commonly suggested. Rather, we can rely on our sense of thirst to keep us hydrated, and we can also choose drinks other than water that contain the nutrients we need to produce energy and keep our cells hydrated.

 

References

Water: More is NOT Better

The recommendation to drink more water is probably the most common and universally agreed upon advice given in the health industry, maybe second only to the suggestion to avoid sugar.

Most everybody has heard that they should start their day with a big glass of water and drink 8 glasses of water a day, and others even suggest that this isn’t enough. Some recommend drinking as much as ½ or even 1 oz of water per pound of bodyweight (this would be 18 glasses of water per day for someone weighing 150 lbs.)

And why wouldn’t we drink that much water?

Water is the essence of life. It has no calories and makes up as much as 60% of our body weight. Plus, it keeps us full so we eat less while also keeping our skin moisturized, wrinkle-free, and glowing. Oh, and did I mention it increases our metabolism too?

Better get chugging…

Yes, that was sarcasm. But it’s allowed because I believed all those things at one point too. For years I was known for never being seen without a water bottle and for getting multiple water refills whenever I was out to eat. I was always drinking water.

But, the dogmatic belief that drinking more water is better for our health is almost entirely unfounded, and most of the research actually points in the opposite direction.

 

The “Benefits” of Drinking More Water

It’s important to first acknowledge that water is not benign. While those that recommend drinking more water often recognize the dangers of dehydration, they ignore the dangers of overhydration. Overhydration can cause many of the same effects as dehydration, including headaches, impaired cognitive function, and even death.

I’ll explain exactly why overhydration is so dangerous in a little bit, but let’s first break down the supposed benefits of drinking water.

First is that water keeps us fuller, causing us to eat less, and has no calories, making it a healthy replacement for beverages that do contain calories. And this is at least somewhat true – drinking more water can make us eat slightly less (1, 2, 3).

But, as you may have read in several of my previous articles, eating less is NOT the answer for fat loss or improved health, and instead leads to stress and degeneration. And, the idea that having calories makes something less healthy is based on the heavily flawed calories-in/calories-out equation, which I described in this article.

The second supposed benefit is that water “increases our metabolism.” Again, this isn’t entirely untrue, as drinking water has been shown to increase energy expenditure by a small amount (around 24 calories per 500 mL) (4). But, this doesn’t mean that it improves metabolic function, will lead to fat loss, or that it’s even beneficial at all. In fact, this increase in energy expenditure is a sign of stress, which I’ll explain further in a little bit.

Third is the assumption that drinking more water increases hydration. Much of the advice to drink more water is based on the idea that dehydration is bad, so drinking water must be good. But, while dehydration is a legitimate issue (although not a very common one), simply drinking lots of water isn’t the best way to solve it.

In order for our cells to use water, they require minerals like sodium, potassium, and magnesium, as well as energy. Water is typically devoid of all those things, so drinking water won’t necessarily increase hydration and can even reduce cellular hydration because it lacks those other important nutrients.

Water is purported to have many other benefits, like relieving headaches and constipation. However, drinking water only helps these symptoms if dehydration was the cause of these symptoms, which often isn’t the case (5, 6). And, if these symptoms weren’t caused by dehydration, drinking water can make them even worse.

Other supposed benefits of drinking lots of water, like “flushing out toxins” and “boosting our immune system,” are mostly fabricated ideas that are, at best, based on a heavily flawed understanding of these features of physiology.

 

Water and Stress

There’s one major problem that comes with drinking lots of water. It’s actually the same issue that causes the extreme effects of overhydration, like headaches, impaired cognitive function, and death, although on a smaller scale.

And that problem is that it dilutes our blood, which reduces the concentration of various electrolytes, most importantly sodium.

The sodium level in our blood is tightly regulated. And, when it drops too low, our body’s stress systems are activated (7, 8). This leads to the production of stress hormones like aldosterone, which cause our bodies to retain more sodium (and excrete less) in order to increase the sodium concentration.

But, retaining sodium comes at a cost – the sodium we would normally excrete in our kidneys is replaced with potassium and magnesium, leading to the loss of greater amounts of these minerals (9).

A lack of potassium and magnesium, as well as the stress hormones themselves, then leads to cell swelling (10, 11, 12, 13). This swelling inhibits our ability to produce and use energy, which is disastrous for every aspect of our health (14).

I explain the cascade of events involved in this adaptive process more thoroughly in this article on salt consumption, but to summarize, a lowered sodium concentration in the blood (either due to drinking too much water or consuming too little sodium), can be extremely stressful on our bodies and has many negative consequences.

And, this is seen quite clearly in the research showing that drinking water increases energy expenditure (these are the studies often cited for water’s ability to “increase our metabolism”).

These studies have shown that this increase in energy expenditure is directly caused by the stress that results from a lowered sodium concentration in the blood (15, 16). This finding has been corroborated by several studies showing that drinking plain water leads to stress but drinking water with enough salt to mimic our normal blood sodium concentrations doesn’t (16, 17, 18, 19).

In other words, forcing ourselves to drink excess water can lead to stress and cell swelling, which negatively affects metabolic function.

But, as I’ll explain in a second, while drinking too much water can be harmful, we don’t have to worry much about it if we simply listen to our body’s innate signals that tell us how much we need to drink.

 

Thirst Has Got You Covered

The moral of the story is that more water is not better. So, there’s no need to force ourselves to drink a certain amount of water each day, which can be far more harmful than helpful. Instead, our bodies have their own hydration sensors that tell us when and how much we need to drink, so we can simply drink when we’re thirsty!

There’s a common myth that by the time you’re feeling thirsty you’re already dehydrated, but this is simply unsupported, as is explained in this quote:

“It is often stated in the lay press (17, 19, 22, 26) and even in professional journals (47) that by the time a person is thirsty that person is already dehydrated. In a number of scientific treatises on thirst, one finds no such assertion (1, 12, 30, 67, 69, 76, 98). On the contrary, a rise in plasma osmolality of less than 2% can elicit thirst, whereas most experts would define dehydration as beginning when a person has lost 3% or more of body weight (96), which translates into a rise in plasma osmolality of at least 5%.” (20)

And, as stated in these quotes, our sense of thirst is extremely sensitive, and it wouldn’t make sense biologically if we had to force ourselves to drink more water than we naturally wanted to just to remain hydrated:

“To prevent dehydration reptiles, birds, vertebrates, and all land animals have evolved an exquisitely sensitive network of physiological controls to maintain body water and fluid intake by thirst.” (6)

“Osmotic regulation of vasopressin secretion and thirst is so sensitive, quick, and accurate (67) that it is hard to imagine that evolutionary development left us with a chronic water deficit that has to be compensated by forcing fluid intake.” (20)

[Note: there’s also a common myth that if your pee isn’t clear you’re dehydrated, but this simply isn’t true (20).]

So, it’s quite clear that by using our sense of thirst, our body’s built-in hydration indicator, we can remain adequately hydrated.

 

Why Water?

There’s no need to limit our beverages to only water. There are tons of other options that come with added nutrients and taste better.

Fruit juice, milk, and tea or coffee with honey or sugar are all great options. These options have nutrients that allow us to produce energy and minerals needed for effective hydration, which water doesn’t have. (If you’re worried about the sugar in these drinks, check out these articles.)

Of course, this doesn’t mean that we need to avoid water, just that other drinks can be even better. And, if we’re drinking more water because we’re sweating a lot or for some other reason, it’s important to make sure we’re also getting enough sodium and other minerals to effectively rehydrate.

 

Just to hammer the point home, forcing ourselves to drink more water is not beneficial for our health, as is commonly suggested. Rather, we can rely on our sense of thirst to keep us hydrated, and we can also choose drinks other than water that contain the nutrients we need to produce energy and keep our cells hydrated.

 

References

Water: More is NOT Better

The recommendation to drink more water is probably the most common and universally agreed upon advice given in the health industry, maybe second only to the suggestion to avoid sugar.

Most everybody has heard that they should start their day with a big glass of water and drink 8 glasses of water a day, and others even suggest that this isn’t enough. Some recommend drinking as much as ½ or even 1 oz of water per pound of bodyweight (this would be 18 glasses of water per day for someone weighing 150 lbs.)

And why wouldn’t we drink that much water?

Water is the essence of life. It has no calories and makes up as much as 60% of our body weight. Plus, it keeps us full so we eat less while also keeping our skin moisturized, wrinkle-free, and glowing. Oh, and did I mention it increases our metabolism too?

Better get chugging…

Yes, that was sarcasm. But it’s allowed because I believed all those things at one point too. For years I was known for never being seen without a water bottle and for getting multiple water refills whenever I was out to eat. I was always drinking water.

But, the dogmatic belief that drinking more water is better for our health is almost entirely unfounded, and most of the research actually points in the opposite direction.

 

The “Benefits” of Drinking More Water

It’s important to first acknowledge that water is not benign. While those that recommend drinking more water often recognize the dangers of dehydration, they ignore the dangers of overhydration. Overhydration can cause many of the same effects as dehydration, including headaches, impaired cognitive function, and even death.

I’ll explain exactly why overhydration is so dangerous in a little bit, but let’s first break down the supposed benefits of drinking water.

First is that water keeps us fuller, causing us to eat less, and has no calories, making it a healthy replacement for beverages that do contain calories. And this is at least somewhat true – drinking more water can make us eat slightly less (1, 2, 3).

But, as you may have read in several of my previous articles, eating less is NOT the answer for fat loss or improved health, and instead leads to stress and degeneration. And, the idea that having calories makes something less healthy is based on the heavily flawed calories-in/calories-out equation, which I described in this article.

The second supposed benefit is that water “increases our metabolism.” Again, this isn’t entirely untrue, as drinking water has been shown to increase energy expenditure by a small amount (around 24 calories per 500 mL) (4). But, this doesn’t mean that it improves metabolic function, will lead to fat loss, or that it’s even beneficial at all. In fact, this increase in energy expenditure is a sign of stress, which I’ll explain further in a little bit.

Third is the assumption that drinking more water increases hydration. Much of the advice to drink more water is based on the idea that dehydration is bad, so drinking water must be good. But, while dehydration is a legitimate issue (although not a very common one), simply drinking lots of water isn’t the best way to solve it.

In order for our cells to use water, they require minerals like sodium, potassium, and magnesium, as well as energy. Water is typically devoid of all those things, so drinking water won’t necessarily increase hydration and can even reduce cellular hydration because it lacks those other important nutrients.

Water is purported to have many other benefits, like relieving headaches and constipation. However, drinking water only helps these symptoms if dehydration was the cause of these symptoms, which often isn’t the case (5, 6). And, if these symptoms weren’t caused by dehydration, drinking water can make them even worse.

Other supposed benefits of drinking lots of water, like “flushing out toxins” and “boosting our immune system,” are mostly fabricated ideas that are, at best, based on a heavily flawed understanding of these features of physiology.

 

Water and Stress

There’s one major problem that comes with drinking lots of water. It’s actually the same issue that causes the extreme effects of overhydration, like headaches, impaired cognitive function, and death, although on a smaller scale.

And that problem is that it dilutes our blood, which reduces the concentration of various electrolytes, most importantly sodium.

The sodium level in our blood is tightly regulated. And, when it drops too low, our body’s stress systems are activated (7, 8). This leads to the production of stress hormones like aldosterone, which cause our bodies to retain more sodium (and excrete less) in order to increase the sodium concentration.

But, retaining sodium comes at a cost – the sodium we would normally excrete in our kidneys is replaced with potassium and magnesium, leading to the loss of greater amounts of these minerals (9).

A lack of potassium and magnesium, as well as the stress hormones themselves, then leads to cell swelling (10, 11, 12, 13). This swelling inhibits our ability to produce and use energy, which is disastrous for every aspect of our health (14).

I explain the cascade of events involved in this adaptive process more thoroughly in this article on salt consumption, but to summarize, a lowered sodium concentration in the blood (either due to drinking too much water or consuming too little sodium), can be extremely stressful on our bodies and has many negative consequences.

And, this is seen quite clearly in the research showing that drinking water increases energy expenditure (these are the studies often cited for water’s ability to “increase our metabolism”).

These studies have shown that this increase in energy expenditure is directly caused by the stress that results from a lowered sodium concentration in the blood (15, 16). This finding has been corroborated by several studies showing that drinking plain water leads to stress but drinking water with enough salt to mimic our normal blood sodium concentrations doesn’t (16, 17, 18, 19).

In other words, forcing ourselves to drink excess water can lead to stress and cell swelling, which negatively affects metabolic function.

But, as I’ll explain in a second, while drinking too much water can be harmful, we don’t have to worry much about it if we simply listen to our body’s innate signals that tell us how much we need to drink.

 

Thirst Has Got You Covered

The moral of the story is that more water is not better. So, there’s no need to force ourselves to drink a certain amount of water each day, which can be far more harmful than helpful. Instead, our bodies have their own hydration sensors that tell us when and how much we need to drink, so we can simply drink when we’re thirsty!

There’s a common myth that by the time you’re feeling thirsty you’re already dehydrated, but this is simply unsupported, as is explained in this quote:

“It is often stated in the lay press (17, 19, 22, 26) and even in professional journals (47) that by the time a person is thirsty that person is already dehydrated. In a number of scientific treatises on thirst, one finds no such assertion (1, 12, 30, 67, 69, 76, 98). On the contrary, a rise in plasma osmolality of less than 2% can elicit thirst, whereas most experts would define dehydration as beginning when a person has lost 3% or more of body weight (96), which translates into a rise in plasma osmolality of at least 5%.” (20)

And, as stated in these quotes, our sense of thirst is extremely sensitive, and it wouldn’t make sense biologically if we had to force ourselves to drink more water than we naturally wanted to just to remain hydrated:

“To prevent dehydration reptiles, birds, vertebrates, and all land animals have evolved an exquisitely sensitive network of physiological controls to maintain body water and fluid intake by thirst.” (6)

“Osmotic regulation of vasopressin secretion and thirst is so sensitive, quick, and accurate (67) that it is hard to imagine that evolutionary development left us with a chronic water deficit that has to be compensated by forcing fluid intake.” (20)

[Note: there’s also a common myth that if your pee isn’t clear you’re dehydrated, but this simply isn’t true (20).]

So, it’s quite clear that by using our sense of thirst, our body’s built-in hydration indicator, we can remain adequately hydrated.

 

Why Water?

There’s no need to limit our beverages to only water. There are tons of other options that come with added nutrients and taste better.

Fruit juice, milk, and tea or coffee with honey or sugar are all great options. These options have nutrients that allow us to produce energy and minerals needed for effective hydration, which water doesn’t have. (If you’re worried about the sugar in these drinks, check out these articles.)

Of course, this doesn’t mean that we need to avoid water, just that other drinks can be even better. And, if we’re drinking more water because we’re sweating a lot or for some other reason, it’s important to make sure we’re also getting enough sodium and other minerals to effectively rehydrate.

 

Just to hammer the point home, forcing ourselves to drink more water is not beneficial for our health, as is commonly suggested. Rather, we can rely on our sense of thirst to keep us hydrated, and we can also choose drinks other than water that contain the nutrients we need to produce energy and keep our cells hydrated.

 

References

Water: More is NOT Better

The recommendation to drink more water is probably the most common and universally agreed upon advice given in the health industry, maybe second only to the suggestion to avoid sugar.

Most everybody has heard that they should start their day with a big glass of water and drink 8 glasses of water a day, and others even suggest that this isn’t enough. Some recommend drinking as much as ½ or even 1 oz of water per pound of bodyweight (this would be 18 glasses of water per day for someone weighing 150 lbs.)

And why wouldn’t we drink that much water?

Water is the essence of life. It has no calories and makes up as much as 60% of our body weight. Plus, it keeps us full so we eat less while also keeping our skin moisturized, wrinkle-free, and glowing. Oh, and did I mention it increases our metabolism too?

Better get chugging…

Yes, that was sarcasm. But it’s allowed because I believed all those things at one point too. For years I was known for never being seen without a water bottle and for getting multiple water refills whenever I was out to eat. I was always drinking water.

But, the dogmatic belief that drinking more water is better for our health is almost entirely unfounded, and most of the research actually points in the opposite direction.

 

The “Benefits” of Drinking More Water

It’s important to first acknowledge that water is not benign. While those that recommend drinking more water often recognize the dangers of dehydration, they ignore the dangers of overhydration. Overhydration can cause many of the same effects as dehydration, including headaches, impaired cognitive function, and even death.

I’ll explain exactly why overhydration is so dangerous in a little bit, but let’s first break down the supposed benefits of drinking water.

First is that water keeps us fuller, causing us to eat less, and has no calories, making it a healthy replacement for beverages that do contain calories. And this is at least somewhat true – drinking more water can make us eat slightly less (1, 2, 3).

But, as you may have read in several of my previous articles, eating less is NOT the answer for fat loss or improved health, and instead leads to stress and degeneration. And, the idea that having calories makes something less healthy is based on the heavily flawed calories-in/calories-out equation, which I described in this article.

The second supposed benefit is that water “increases our metabolism.” Again, this isn’t entirely untrue, as drinking water has been shown to increase energy expenditure by a small amount (around 24 calories per 500 mL) (4). But, this doesn’t mean that it improves metabolic function, will lead to fat loss, or that it’s even beneficial at all. In fact, this increase in energy expenditure is a sign of stress, which I’ll explain further in a little bit.

Third is the assumption that drinking more water increases hydration. Much of the advice to drink more water is based on the idea that dehydration is bad, so drinking water must be good. But, while dehydration is a legitimate issue (although not a very common one), simply drinking lots of water isn’t the best way to solve it.

In order for our cells to use water, they require minerals like sodium, potassium, and magnesium, as well as energy. Water is typically devoid of all those things, so drinking water won’t necessarily increase hydration and can even reduce cellular hydration because it lacks those other important nutrients.

Water is purported to have many other benefits, like relieving headaches and constipation. However, drinking water only helps these symptoms if dehydration was the cause of these symptoms, which often isn’t the case (5, 6). And, if these symptoms weren’t caused by dehydration, drinking water can make them even worse.

Other supposed benefits of drinking lots of water, like “flushing out toxins” and “boosting our immune system,” are mostly fabricated ideas that are, at best, based on a heavily flawed understanding of these features of physiology.

 

Water and Stress

There’s one major problem that comes with drinking lots of water. It’s actually the same issue that causes the extreme effects of overhydration, like headaches, impaired cognitive function, and death, although on a smaller scale.

And that problem is that it dilutes our blood, which reduces the concentration of various electrolytes, most importantly sodium.

The sodium level in our blood is tightly regulated. And, when it drops too low, our body’s stress systems are activated (7, 8). This leads to the production of stress hormones like aldosterone, which cause our bodies to retain more sodium (and excrete less) in order to increase the sodium concentration.

But, retaining sodium comes at a cost – the sodium we would normally excrete in our kidneys is replaced with potassium and magnesium, leading to the loss of greater amounts of these minerals (9).

A lack of potassium and magnesium, as well as the stress hormones themselves, then leads to cell swelling (10, 11, 12, 13). This swelling inhibits our ability to produce and use energy, which is disastrous for every aspect of our health (14).

I explain the cascade of events involved in this adaptive process more thoroughly in this article on salt consumption, but to summarize, a lowered sodium concentration in the blood (either due to drinking too much water or consuming too little sodium), can be extremely stressful on our bodies and has many negative consequences.

And, this is seen quite clearly in the research showing that drinking water increases energy expenditure (these are the studies often cited for water’s ability to “increase our metabolism”).

These studies have shown that this increase in energy expenditure is directly caused by the stress that results from a lowered sodium concentration in the blood (15, 16). This finding has been corroborated by several studies showing that drinking plain water leads to stress but drinking water with enough salt to mimic our normal blood sodium concentrations doesn’t (16, 17, 18, 19).

In other words, forcing ourselves to drink excess water can lead to stress and cell swelling, which negatively affects metabolic function.

But, as I’ll explain in a second, while drinking too much water can be harmful, we don’t have to worry much about it if we simply listen to our body’s innate signals that tell us how much we need to drink.

 

Thirst Has Got You Covered

The moral of the story is that more water is not better. So, there’s no need to force ourselves to drink a certain amount of water each day, which can be far more harmful than helpful. Instead, our bodies have their own hydration sensors that tell us when and how much we need to drink, so we can simply drink when we’re thirsty!

There’s a common myth that by the time you’re feeling thirsty you’re already dehydrated, but this is simply unsupported, as is explained in this quote:

“It is often stated in the lay press (17, 19, 22, 26) and even in professional journals (47) that by the time a person is thirsty that person is already dehydrated. In a number of scientific treatises on thirst, one finds no such assertion (1, 12, 30, 67, 69, 76, 98). On the contrary, a rise in plasma osmolality of less than 2% can elicit thirst, whereas most experts would define dehydration as beginning when a person has lost 3% or more of body weight (96), which translates into a rise in plasma osmolality of at least 5%.” (20)

And, as stated in these quotes, our sense of thirst is extremely sensitive, and it wouldn’t make sense biologically if we had to force ourselves to drink more water than we naturally wanted to just to remain hydrated:

“To prevent dehydration reptiles, birds, vertebrates, and all land animals have evolved an exquisitely sensitive network of physiological controls to maintain body water and fluid intake by thirst.” (6)

“Osmotic regulation of vasopressin secretion and thirst is so sensitive, quick, and accurate (67) that it is hard to imagine that evolutionary development left us with a chronic water deficit that has to be compensated by forcing fluid intake.” (20)

[Note: there’s also a common myth that if your pee isn’t clear you’re dehydrated, but this simply isn’t true (20).]

So, it’s quite clear that by using our sense of thirst, our body’s built-in hydration indicator, we can remain adequately hydrated.

 

Why Water?

There’s no need to limit our beverages to only water. There are tons of other options that come with added nutrients and taste better.

Fruit juice, milk, and tea or coffee with honey or sugar are all great options. These options have nutrients that allow us to produce energy and minerals needed for effective hydration, which water doesn’t have. (If you’re worried about the sugar in these drinks, check out these articles.)

Of course, this doesn’t mean that we need to avoid water, just that other drinks can be even better. And, if we’re drinking more water because we’re sweating a lot or for some other reason, it’s important to make sure we’re also getting enough sodium and other minerals to effectively rehydrate.

 

Just to hammer the point home, forcing ourselves to drink more water is not beneficial for our health, as is commonly suggested. Rather, we can rely on our sense of thirst to keep us hydrated, and we can also choose drinks other than water that contain the nutrients we need to produce energy and keep our cells hydrated.

 

References

Water: More is NOT Better

The recommendation to drink more water is probably the most common and universally agreed upon advice given in the health industry, maybe second only to the suggestion to avoid sugar.

Most everybody has heard that they should start their day with a big glass of water and drink 8 glasses of water a day, and others even suggest that this isn’t enough. Some recommend drinking as much as ½ or even 1 oz of water per pound of bodyweight (this would be 18 glasses of water per day for someone weighing 150 lbs.)

And why wouldn’t we drink that much water?

Water is the essence of life. It has no calories and makes up as much as 60% of our body weight. Plus, it keeps us full so we eat less while also keeping our skin moisturized, wrinkle-free, and glowing. Oh, and did I mention it increases our metabolism too?

Better get chugging…

Yes, that was sarcasm. But it’s allowed because I believed all those things at one point too. For years I was known for never being seen without a water bottle and for getting multiple water refills whenever I was out to eat. I was always drinking water.

But, the dogmatic belief that drinking more water is better for our health is almost entirely unfounded, and most of the research actually points in the opposite direction.

 

The “Benefits” of Drinking More Water

It’s important to first acknowledge that water is not benign. While those that recommend drinking more water often recognize the dangers of dehydration, they ignore the dangers of overhydration. Overhydration can cause many of the same effects as dehydration, including headaches, impaired cognitive function, and even death.

I’ll explain exactly why overhydration is so dangerous in a little bit, but let’s first break down the supposed benefits of drinking water.

First is that water keeps us fuller, causing us to eat less, and has no calories, making it a healthy replacement for beverages that do contain calories. And this is at least somewhat true – drinking more water can make us eat slightly less (1, 2, 3).

But, as you may have read in several of my previous articles, eating less is NOT the answer for fat loss or improved health, and instead leads to stress and degeneration. And, the idea that having calories makes something less healthy is based on the heavily flawed calories-in/calories-out equation, which I described in this article.

The second supposed benefit is that water “increases our metabolism.” Again, this isn’t entirely untrue, as drinking water has been shown to increase energy expenditure by a small amount (around 24 calories per 500 mL) (4). But, this doesn’t mean that it improves metabolic function, will lead to fat loss, or that it’s even beneficial at all. In fact, this increase in energy expenditure is a sign of stress, which I’ll explain further in a little bit.

Third is the assumption that drinking more water increases hydration. Much of the advice to drink more water is based on the idea that dehydration is bad, so drinking water must be good. But, while dehydration is a legitimate issue (although not a very common one), simply drinking lots of water isn’t the best way to solve it.

In order for our cells to use water, they require minerals like sodium, potassium, and magnesium, as well as energy. Water is typically devoid of all those things, so drinking water won’t necessarily increase hydration and can even reduce cellular hydration because it lacks those other important nutrients.

Water is purported to have many other benefits, like relieving headaches and constipation. However, drinking water only helps these symptoms if dehydration was the cause of these symptoms, which often isn’t the case (5, 6). And, if these symptoms weren’t caused by dehydration, drinking water can make them even worse.

Other supposed benefits of drinking lots of water, like “flushing out toxins” and “boosting our immune system,” are mostly fabricated ideas that are, at best, based on a heavily flawed understanding of these features of physiology.

 

Water and Stress

There’s one major problem that comes with drinking lots of water. It’s actually the same issue that causes the extreme effects of overhydration, like headaches, impaired cognitive function, and death, although on a smaller scale.

And that problem is that it dilutes our blood, which reduces the concentration of various electrolytes, most importantly sodium.

The sodium level in our blood is tightly regulated. And, when it drops too low, our body’s stress systems are activated (7, 8). This leads to the production of stress hormones like aldosterone, which cause our bodies to retain more sodium (and excrete less) in order to increase the sodium concentration.

But, retaining sodium comes at a cost – the sodium we would normally excrete in our kidneys is replaced with potassium and magnesium, leading to the loss of greater amounts of these minerals (9).

A lack of potassium and magnesium, as well as the stress hormones themselves, then leads to cell swelling (10, 11, 12, 13). This swelling inhibits our ability to produce and use energy, which is disastrous for every aspect of our health (14).

I explain the cascade of events involved in this adaptive process more thoroughly in this article on salt consumption, but to summarize, a lowered sodium concentration in the blood (either due to drinking too much water or consuming too little sodium), can be extremely stressful on our bodies and has many negative consequences.

And, this is seen quite clearly in the research showing that drinking water increases energy expenditure (these are the studies often cited for water’s ability to “increase our metabolism”).

These studies have shown that this increase in energy expenditure is directly caused by the stress that results from a lowered sodium concentration in the blood (15, 16). This finding has been corroborated by several studies showing that drinking plain water leads to stress but drinking water with enough salt to mimic our normal blood sodium concentrations doesn’t (16, 17, 18, 19).

In other words, forcing ourselves to drink excess water can lead to stress and cell swelling, which negatively affects metabolic function.

But, as I’ll explain in a second, while drinking too much water can be harmful, we don’t have to worry much about it if we simply listen to our body’s innate signals that tell us how much we need to drink.

 

Thirst Has Got You Covered

The moral of the story is that more water is not better. So, there’s no need to force ourselves to drink a certain amount of water each day, which can be far more harmful than helpful. Instead, our bodies have their own hydration sensors that tell us when and how much we need to drink, so we can simply drink when we’re thirsty!

There’s a common myth that by the time you’re feeling thirsty you’re already dehydrated, but this is simply unsupported, as is explained in this quote:

“It is often stated in the lay press (17, 19, 22, 26) and even in professional journals (47) that by the time a person is thirsty that person is already dehydrated. In a number of scientific treatises on thirst, one finds no such assertion (1, 12, 30, 67, 69, 76, 98). On the contrary, a rise in plasma osmolality of less than 2% can elicit thirst, whereas most experts would define dehydration as beginning when a person has lost 3% or more of body weight (96), which translates into a rise in plasma osmolality of at least 5%.” (20)

And, as stated in these quotes, our sense of thirst is extremely sensitive, and it wouldn’t make sense biologically if we had to force ourselves to drink more water than we naturally wanted to just to remain hydrated:

“To prevent dehydration reptiles, birds, vertebrates, and all land animals have evolved an exquisitely sensitive network of physiological controls to maintain body water and fluid intake by thirst.” (6)

“Osmotic regulation of vasopressin secretion and thirst is so sensitive, quick, and accurate (67) that it is hard to imagine that evolutionary development left us with a chronic water deficit that has to be compensated by forcing fluid intake.” (20)

[Note: there’s also a common myth that if your pee isn’t clear you’re dehydrated, but this simply isn’t true (20).]

So, it’s quite clear that by using our sense of thirst, our body’s built-in hydration indicator, we can remain adequately hydrated.

 

Why Water?

There’s no need to limit our beverages to only water. There are tons of other options that come with added nutrients and taste better.

Fruit juice, milk, and tea or coffee with honey or sugar are all great options. These options have nutrients that allow us to produce energy and minerals needed for effective hydration, which water doesn’t have. (If you’re worried about the sugar in these drinks, check out these articles.)

Of course, this doesn’t mean that we need to avoid water, just that other drinks can be even better. And, if we’re drinking more water because we’re sweating a lot or for some other reason, it’s important to make sure we’re also getting enough sodium and other minerals to effectively rehydrate.

 

Just to hammer the point home, forcing ourselves to drink more water is not beneficial for our health, as is commonly suggested. Rather, we can rely on our sense of thirst to keep us hydrated, and we can also choose drinks other than water that contain the nutrients we need to produce energy and keep our cells hydrated.

 

References

The True Cause of Type 2 Diabetes and Insulin Resistance

studies cited and relevant articles

The True Cause of Type 2 Diabetes and Insulin Resistance

studies cited and relevant articles

The True Cause of Type 2 Diabetes and Insulin Resistance

studies cited and relevant articles

The True Cause of Type 2 Diabetes and Insulin Resistance

studies cited and relevant articles

The True Cause of Type 2 Diabetes and Insulin Resistance

studies cited and relevant articles

The True Cause of Type 2 Diabetes and Insulin Resistance

studies cited and relevant articles

The True Cause of Type 2 Diabetes and Insulin Resistance

studies cited and relevant articles

The True Cause of Type 2 Diabetes and Insulin Resistance

studies cited and relevant articles

Aging, Metabolism, and Caloric Restriction

Live fast and die young,” “the flame that burns twice as bright burns half as long,” “don’t burn the candle at both ends.”

These phrases embody the idea that our resources are limited, and the faster we use them the sooner they, and we, are gone.

For a while, a similar idea prevailed in biology and medicine that suggested that we would live longer if we reduced the amount of energy we produced and used, as is explained in this quote:

“The idea that aging should be linked to energy expenditure has a long history that can be traced to the late 1800s and the industrial revolution. Machines that are run fast wear out more quickly, so the notion was born that humans and animals might experience similar fates: the faster they live (expressed as greater energy expenditure), the sooner they die.” (1)

The rate of living theory was born out of this mechanical view of biology and states that the greater an organism’s energy expenditure, the shorter it’s lifespan. It has since been expanded to suggest that aging, health, and lifespan are tied to energy expenditure.

This theory has been primarily supported by the evidence that animals with lower metabolic rates relative to their body mass have longer lifespans and that low-calorie diets extend lifespan by reducing the metabolic rate. But, it turns out it’s not quite that simple.

 

Aging and Metabolism

The concept that animals with higher metabolic rates have shorter lives isn’t particularly noteworthy. It’s now common knowledge that small animals, like mice, typically have high metabolic rates (relative to their size) and short lifespans, while large animals, like elephants, typically have low metabolic rates (relative to their size) and long lifespans.

This finding that species’ metabolic rates correlate with their lifespans corroborated the rate of living theory. However, while it was originally assumed that the metabolic rate was responsible for the rate of aging, we’ve since learned that there are other factors that explain this finding (1, 2).

The most notable of these factors is the composition of the cellular and mitochondrial phospholipid membranes (3, 4) [Note: while there’s substantial evidence that these “membranes” may not exist, the same principle applies to the composition of the non-membrane lipid structural components]. These membranes play a vital role in the production and usage of energy.

The fatty acids that make up these membranes vary in terms of their saturation. The more saturated the fatty acids are, the more structurally stable they are. Weaker, more unsaturated membranes are more susceptible to damage and have a higher permeability to protons and ions (3, 4, 5).

When the fatty acids in these membranes become damaged, they increase oxidative stress which damages all parts of our cells, including their protein structure, fatty acids, and DNA (3). This impairs energy production and requires energy for repair, making it doubly wasteful.

And, the increased permeability to protons and ions reduces the production of usable energy and increases the production of heat, which effectively reduces the efficiency of energy production (5). The increased permeability also increases the activity of Na+/K+ ATPase and proton pumps, which increases the energy demand (5) [Note: while there’s substantial evidence that these “pumps” may not exist, the same principle of an increased energy demand still applies].

Together, the differences in oxidative damage, wasting of energy, and efficiency of energy production due to differences in membrane saturation account for the differences in metabolic rates between species as well as the differences in aging and lifespan (3, 4).

In other words, species that have more saturated membranes are more energetically efficient and this results in slower aging.

And, what’s even more remarkable is that within species, where the membrane saturation is typically constant, those with the highest metabolic rates relative to their body weight actually live the longest (1, 2, 3). This supports the directly opposite conclusion of the rate of living theory: producing and using more energy slows aging and extends lifespan.

 

Aging and Caloric Restriction

Now, what about all those caloric restriction studies that show that eating less reduces the metabolic rate and increases lifespan?

While reducing caloric intake has been shown to reliably increase lifespan while also slowing the metabolic rate, there’s now considerable evidence that factors other than the reduction in metabolic rate are responsible for the life-extending effects of these calorie-restricting-diets.

Firstly, these caloric restriction studies are often performed by splitting the subjects into a caloric restriction group and a control group that eats ad-libitum (meaning they can eat as much as they want). This presents a problem because the subjects fed ad-libitum become overweight and are prone to the early onset of diseases and death, making them poor controls.

In fact, the supposed life-extending effects of caloric restriction are directly related to weight gain in the ad-libitum control groups (6). In other words, the less weight gain there is in the control group, the less life-extending effects are seen in the caloric restriction group. This suggests that the “life-extending effects” seen in the caloric restriction groups are simply due to life-shortening effects of the control groups.

Secondly, caloric restriction inherently reduces the consumption of amino acids that have been shown to reduce longevity and increase oxidative damage, including methionine, cysteine, and tryptophan. It’s been shown that the life-extending effects of caloric restriction can be entirely accounted for by the reduction of these amino acids in the diet (7, 8, 9, 10).

In other words, simply reducing the consumption of these amino acids without reducing caloric intake results in the same life-extending effects. These effects on aging can at least partially be accounted for by changes in membrane saturation, which I explained earlier is the primary determinant of lifespan between species (8).

Lastly, caloric restriction also inherently reduces the consumption of polyunsaturated fatty acids (PUFA). PUFA consumption is also directly related to membrane unsaturation, which accounts for many of its effects on aging, health, and lifespan. (I’ve written about PUFA’s negative effects on energy balance here and here.)

So, while it hasn’t been directly studied in this context, a reduction in PUFA consumption is likely another factor that accounts for the life-extending effects of caloric restriction.

All three of these factors are corroborated by other studies showing that reductions in the metabolic rate are not responsible for the life-extending effects of caloric restriction (11, 12) and that reductions in membrane unsaturation are (3, 13, 14, 15).

 

The More Energy The Better

Now that it’s known that a faster metabolic rate is not the cause of a shorter lifespan, the popular narrative can be flipped on its head: running the human “machine” faster does not cause it to deteriorate quicker. Instead, the opposite is true.

As I’ve outlined in this article, energy is the driving force behind our health and all our bodily functions. From this bioenergetic view of health, it’s evident that the production of adequate amounts of energy is what allows for regeneration, rather than the deterioration and degeneration we see when energy production is impaired, such as in disease and aging.

Of course, this capacity for growth and regeneration isn’t compatible with a mechanical view of the human organism, further illustrating one of its many flaws.

 

As I’ve mentioned before, improving energy production is much easier said than done, as this process can be inhibited by various factors. I outline several of the key factors affecting energy production and usage, how they affect our health, and what you can do about them in my free health and energy balance mini-course, which you can sign up for below.

 

References

Aging, Metabolism, and Caloric Restriction

Live fast and die young,” “the flame that burns twice as bright burns half as long,” “don’t burn the candle at both ends.”

These phrases embody the idea that our resources are limited, and the faster we use them the sooner they, and we, are gone.

For a while, a similar idea prevailed in biology and medicine that suggested that we would live longer if we reduced the amount of energy we produced and used, as is explained in this quote:

“The idea that aging should be linked to energy expenditure has a long history that can be traced to the late 1800s and the industrial revolution. Machines that are run fast wear out more quickly, so the notion was born that humans and animals might experience similar fates: the faster they live (expressed as greater energy expenditure), the sooner they die.” (1)

The rate of living theory was born out of this mechanical view of biology and states that the greater an organism’s energy expenditure, the shorter it’s lifespan. It has since been expanded to suggest that aging, health, and lifespan are tied to energy expenditure.

This theory has been primarily supported by the evidence that animals with lower metabolic rates relative to their body mass have longer lifespans and that low-calorie diets extend lifespan by reducing the metabolic rate. But, it turns out it’s not quite that simple.

 

Aging and Metabolism

The concept that animals with higher metabolic rates have shorter lives isn’t particularly noteworthy. It’s now common knowledge that small animals, like mice, typically have high metabolic rates (relative to their size) and short lifespans, while large animals, like elephants, typically have low metabolic rates (relative to their size) and long lifespans.

This finding that species’ metabolic rates correlate with their lifespans corroborated the rate of living theory. However, while it was originally assumed that the metabolic rate was responsible for the rate of aging, we’ve since learned that there are other factors that explain this finding (1, 2).

The most notable of these factors is the composition of the cellular and mitochondrial phospholipid membranes (3, 4) [Note: while there’s substantial evidence that these “membranes” may not exist, the same principle applies to the composition of the non-membrane lipid structural components]. These membranes play a vital role in the production and usage of energy.

The fatty acids that make up these membranes vary in terms of their saturation. The more saturated the fatty acids are, the more structurally stable they are. Weaker, more unsaturated membranes are more susceptible to damage and have a higher permeability to protons and ions (3, 4, 5).

When the fatty acids in these membranes become damaged, they increase oxidative stress which damages all parts of our cells, including their protein structure, fatty acids, and DNA (3). This impairs energy production and requires energy for repair, making it doubly wasteful.

And, the increased permeability to protons and ions reduces the production of usable energy and increases the production of heat, which effectively reduces the efficiency of energy production (5). The increased permeability also increases the activity of Na+/K+ ATPase and proton pumps, which increases the energy demand (5) [Note: while there’s substantial evidence that these “pumps” may not exist, the same principle of an increased energy demand still applies].

Together, the differences in oxidative damage, wasting of energy, and efficiency of energy production due to differences in membrane saturation account for the differences in metabolic rates between species as well as the differences in aging and lifespan (3, 4).

In other words, species that have more saturated membranes are more energetically efficient and this results in slower aging.

And, what’s even more remarkable is that within species, where the membrane saturation is typically constant, those with the highest metabolic rates relative to their body weight actually live the longest (1, 2, 3). This supports the directly opposite conclusion of the rate of living theory: producing and using more energy slows aging and extends lifespan.

 

Aging and Caloric Restriction

Now, what about all those caloric restriction studies that show that eating less reduces the metabolic rate and increases lifespan?

While reducing caloric intake has been shown to reliably increase lifespan while also slowing the metabolic rate, there’s now considerable evidence that factors other than the reduction in metabolic rate are responsible for the life-extending effects of these calorie-restricting-diets.

Firstly, these caloric restriction studies are often performed by splitting the subjects into a caloric restriction group and a control group that eats ad-libitum (meaning they can eat as much as they want). This presents a problem because the subjects fed ad-libitum become overweight and are prone to the early onset of diseases and death, making them poor controls.

In fact, the supposed life-extending effects of caloric restriction are directly related to weight gain in the ad-libitum control groups (6). In other words, the less weight gain there is in the control group, the less life-extending effects are seen in the caloric restriction group. This suggests that the “life-extending effects” seen in the caloric restriction groups are simply due to life-shortening effects of the control groups.

Secondly, caloric restriction inherently reduces the consumption of amino acids that have been shown to reduce longevity and increase oxidative damage, including methionine, cysteine, and tryptophan. It’s been shown that the life-extending effects of caloric restriction can be entirely accounted for by the reduction of these amino acids in the diet (7, 8, 9, 10).

In other words, simply reducing the consumption of these amino acids without reducing caloric intake results in the same life-extending effects. These effects on aging can at least partially be accounted for by changes in membrane saturation, which I explained earlier is the primary determinant of lifespan between species (8).

Lastly, caloric restriction also inherently reduces the consumption of polyunsaturated fatty acids (PUFA). PUFA consumption is also directly related to membrane unsaturation, which accounts for many of its effects on aging, health, and lifespan. (I’ve written about PUFA’s negative effects on energy balance here and here.)

So, while it hasn’t been directly studied in this context, a reduction in PUFA consumption is likely another factor that accounts for the life-extending effects of caloric restriction.

All three of these factors are corroborated by other studies showing that reductions in the metabolic rate are not responsible for the life-extending effects of caloric restriction (11, 12) and that reductions in membrane unsaturation are (3, 13, 14, 15).

 

The More Energy The Better

Now that it’s known that a faster metabolic rate is not the cause of a shorter lifespan, the popular narrative can be flipped on its head: running the human “machine” faster does not cause it to deteriorate quicker. Instead, the opposite is true.

As I’ve outlined in this article, energy is the driving force behind our health and all our bodily functions. From this bioenergetic view of health, it’s evident that the production of adequate amounts of energy is what allows for regeneration, rather than the deterioration and degeneration we see when energy production is impaired, such as in disease and aging.

Of course, this capacity for growth and regeneration isn’t compatible with a mechanical view of the human organism, further illustrating one of its many flaws.

 

As I’ve mentioned before, improving energy production is much easier said than done, as this process can be inhibited by various factors. I outline several of the key factors affecting energy production and usage, how they affect our health, and what you can do about them in my free health and energy balance mini-course, which you can sign up for below.

 

References

Aging, Metabolism, and Caloric Restriction

Live fast and die young,” “the flame that burns twice as bright burns half as long,” “don’t burn the candle at both ends.”

These phrases embody the idea that our resources are limited, and the faster we use them the sooner they, and we, are gone.

For a while, a similar idea prevailed in biology and medicine that suggested that we would live longer if we reduced the amount of energy we produced and used, as is explained in this quote:

“The idea that aging should be linked to energy expenditure has a long history that can be traced to the late 1800s and the industrial revolution. Machines that are run fast wear out more quickly, so the notion was born that humans and animals might experience similar fates: the faster they live (expressed as greater energy expenditure), the sooner they die.” (1)

The rate of living theory was born out of this mechanical view of biology and states that the greater an organism’s energy expenditure, the shorter it’s lifespan. It has since been expanded to suggest that aging, health, and lifespan are tied to energy expenditure.

This theory has been primarily supported by the evidence that animals with lower metabolic rates relative to their body mass have longer lifespans and that low-calorie diets extend lifespan by reducing the metabolic rate. But, it turns out it’s not quite that simple.

 

Aging and Metabolism

The concept that animals with higher metabolic rates have shorter lives isn’t particularly noteworthy. It’s now common knowledge that small animals, like mice, typically have high metabolic rates (relative to their size) and short lifespans, while large animals, like elephants, typically have low metabolic rates (relative to their size) and long lifespans.

This finding that species’ metabolic rates correlate with their lifespans corroborated the rate of living theory. However, while it was originally assumed that the metabolic rate was responsible for the rate of aging, we’ve since learned that there are other factors that explain this finding (1, 2).

The most notable of these factors is the composition of the cellular and mitochondrial phospholipid membranes (3, 4) [Note: while there’s substantial evidence that these “membranes” may not exist, the same principle applies to the composition of the non-membrane lipid structural components]. These membranes play a vital role in the production and usage of energy.

The fatty acids that make up these membranes vary in terms of their saturation. The more saturated the fatty acids are, the more structurally stable they are. Weaker, more unsaturated membranes are more susceptible to damage and have a higher permeability to protons and ions (3, 4, 5).

When the fatty acids in these membranes become damaged, they increase oxidative stress which damages all parts of our cells, including their protein structure, fatty acids, and DNA (3). This impairs energy production and requires energy for repair, making it doubly wasteful.

And, the increased permeability to protons and ions reduces the production of usable energy and increases the production of heat, which effectively reduces the efficiency of energy production (5). The increased permeability also increases the activity of Na+/K+ ATPase and proton pumps, which increases the energy demand (5) [Note: while there’s substantial evidence that these “pumps” may not exist, the same principle of an increased energy demand still applies].

Together, the differences in oxidative damage, wasting of energy, and efficiency of energy production due to differences in membrane saturation account for the differences in metabolic rates between species as well as the differences in aging and lifespan (3, 4).

In other words, species that have more saturated membranes are more energetically efficient and this results in slower aging.

And, what’s even more remarkable is that within species, where the membrane saturation is typically constant, those with the highest metabolic rates relative to their body weight actually live the longest (1, 2, 3). This supports the directly opposite conclusion of the rate of living theory: producing and using more energy slows aging and extends lifespan.

 

Aging and Caloric Restriction

Now, what about all those caloric restriction studies that show that eating less reduces the metabolic rate and increases lifespan?

While reducing caloric intake has been shown to reliably increase lifespan while also slowing the metabolic rate, there’s now considerable evidence that factors other than the reduction in metabolic rate are responsible for the life-extending effects of these calorie-restricting-diets.

Firstly, these caloric restriction studies are often performed by splitting the subjects into a caloric restriction group and a control group that eats ad-libitum (meaning they can eat as much as they want). This presents a problem because the subjects fed ad-libitum become overweight and are prone to the early onset of diseases and death, making them poor controls.

In fact, the supposed life-extending effects of caloric restriction are directly related to weight gain in the ad-libitum control groups (6). In other words, the less weight gain there is in the control group, the less life-extending effects are seen in the caloric restriction group. This suggests that the “life-extending effects” seen in the caloric restriction groups are simply due to life-shortening effects of the control groups.

Secondly, caloric restriction inherently reduces the consumption of amino acids that have been shown to reduce longevity and increase oxidative damage, including methionine, cysteine, and tryptophan. It’s been shown that the life-extending effects of caloric restriction can be entirely accounted for by the reduction of these amino acids in the diet (7, 8, 9, 10).

In other words, simply reducing the consumption of these amino acids without reducing caloric intake results in the same life-extending effects. These effects on aging can at least partially be accounted for by changes in membrane saturation, which I explained earlier is the primary determinant of lifespan between species (8).

Lastly, caloric restriction also inherently reduces the consumption of polyunsaturated fatty acids (PUFA). PUFA consumption is also directly related to membrane unsaturation, which accounts for many of its effects on aging, health, and lifespan. (I’ve written about PUFA’s negative effects on energy balance here and here.)

So, while it hasn’t been directly studied in this context, a reduction in PUFA consumption is likely another factor that accounts for the life-extending effects of caloric restriction.

All three of these factors are corroborated by other studies showing that reductions in the metabolic rate are not responsible for the life-extending effects of caloric restriction (11, 12) and that reductions in membrane unsaturation are (3, 13, 14, 15).

 

The More Energy The Better

Now that it’s known that a faster metabolic rate is not the cause of a shorter lifespan, the popular narrative can be flipped on its head: running the human “machine” faster does not cause it to deteriorate quicker. Instead, the opposite is true.

As I’ve outlined in this article, energy is the driving force behind our health and all our bodily functions. From this bioenergetic view of health, it’s evident that the production of adequate amounts of energy is what allows for regeneration, rather than the deterioration and degeneration we see when energy production is impaired, such as in disease and aging.

Of course, this capacity for growth and regeneration isn’t compatible with a mechanical view of the human organism, further illustrating one of its many flaws.

 

As I’ve mentioned before, improving energy production is much easier said than done, as this process can be inhibited by various factors. I outline several of the key factors affecting energy production and usage, how they affect our health, and what you can do about them in my free health and energy balance mini-course, which you can sign up for below.

 

References

Aging, Metabolism, and Caloric Restriction

Live fast and die young,” “the flame that burns twice as bright burns half as long,” “don’t burn the candle at both ends.”

These phrases embody the idea that our resources are limited, and the faster we use them the sooner they, and we, are gone.

For a while, a similar idea prevailed in biology and medicine that suggested that we would live longer if we reduced the amount of energy we produced and used, as is explained in this quote:

“The idea that aging should be linked to energy expenditure has a long history that can be traced to the late 1800s and the industrial revolution. Machines that are run fast wear out more quickly, so the notion was born that humans and animals might experience similar fates: the faster they live (expressed as greater energy expenditure), the sooner they die.” (1)

The rate of living theory was born out of this mechanical view of biology and states that the greater an organism’s energy expenditure, the shorter it’s lifespan. It has since been expanded to suggest that aging, health, and lifespan are tied to energy expenditure.

This theory has been primarily supported by the evidence that animals with lower metabolic rates relative to their body mass have longer lifespans and that low-calorie diets extend lifespan by reducing the metabolic rate. But, it turns out it’s not quite that simple.

 

Aging and Metabolism

The concept that animals with higher metabolic rates have shorter lives isn’t particularly noteworthy. It’s now common knowledge that small animals, like mice, typically have high metabolic rates (relative to their size) and short lifespans, while large animals, like elephants, typically have low metabolic rates (relative to their size) and long lifespans.

This finding that species’ metabolic rates correlate with their lifespans corroborated the rate of living theory. However, while it was originally assumed that the metabolic rate was responsible for the rate of aging, we’ve since learned that there are other factors that explain this finding (1, 2).

The most notable of these factors is the composition of the cellular and mitochondrial phospholipid membranes (3, 4) [Note: while there’s substantial evidence that these “membranes” may not exist, the same principle applies to the composition of the non-membrane lipid structural components]. These membranes play a vital role in the production and usage of energy.

The fatty acids that make up these membranes vary in terms of their saturation. The more saturated the fatty acids are, the more structurally stable they are. Weaker, more unsaturated membranes are more susceptible to damage and have a higher permeability to protons and ions (3, 4, 5).

When the fatty acids in these membranes become damaged, they increase oxidative stress which damages all parts of our cells, including their protein structure, fatty acids, and DNA (3). This impairs energy production and requires energy for repair, making it doubly wasteful.

And, the increased permeability to protons and ions reduces the production of usable energy and increases the production of heat, which effectively reduces the efficiency of energy production (5). The increased permeability also increases the activity of Na+/K+ ATPase and proton pumps, which increases the energy demand (5) [Note: while there’s substantial evidence that these “pumps” may not exist, the same principle of an increased energy demand still applies].

Together, the differences in oxidative damage, wasting of energy, and efficiency of energy production due to differences in membrane saturation account for the differences in metabolic rates between species as well as the differences in aging and lifespan (3, 4).

In other words, species that have more saturated membranes are more energetically efficient and this results in slower aging.

And, what’s even more remarkable is that within species, where the membrane saturation is typically constant, those with the highest metabolic rates relative to their body weight actually live the longest (1, 2, 3). This supports the directly opposite conclusion of the rate of living theory: producing and using more energy slows aging and extends lifespan.

 

Aging and Caloric Restriction

Now, what about all those caloric restriction studies that show that eating less reduces the metabolic rate and increases lifespan?

While reducing caloric intake has been shown to reliably increase lifespan while also slowing the metabolic rate, there’s now considerable evidence that factors other than the reduction in metabolic rate are responsible for the life-extending effects of these calorie-restricting-diets.

Firstly, these caloric restriction studies are often performed by splitting the subjects into a caloric restriction group and a control group that eats ad-libitum (meaning they can eat as much as they want). This presents a problem because the subjects fed ad-libitum become overweight and are prone to the early onset of diseases and death, making them poor controls.

In fact, the supposed life-extending effects of caloric restriction are directly related to weight gain in the ad-libitum control groups (6). In other words, the less weight gain there is in the control group, the less life-extending effects are seen in the caloric restriction group. This suggests that the “life-extending effects” seen in the caloric restriction groups are simply due to life-shortening effects of the control groups.

Secondly, caloric restriction inherently reduces the consumption of amino acids that have been shown to reduce longevity and increase oxidative damage, including methionine, cysteine, and tryptophan. It’s been shown that the life-extending effects of caloric restriction can be entirely accounted for by the reduction of these amino acids in the diet (7, 8, 9, 10).

In other words, simply reducing the consumption of these amino acids without reducing caloric intake results in the same life-extending effects. These effects on aging can at least partially be accounted for by changes in membrane saturation, which I explained earlier is the primary determinant of lifespan between species (8).

Lastly, caloric restriction also inherently reduces the consumption of polyunsaturated fatty acids (PUFA). PUFA consumption is also directly related to membrane unsaturation, which accounts for many of its effects on aging, health, and lifespan. (I’ve written about PUFA’s negative effects on energy balance here and here.)

So, while it hasn’t been directly studied in this context, a reduction in PUFA consumption is likely another factor that accounts for the life-extending effects of caloric restriction.

All three of these factors are corroborated by other studies showing that reductions in the metabolic rate are not responsible for the life-extending effects of caloric restriction (11, 12) and that reductions in membrane unsaturation are (3, 13, 14, 15).

 

The More Energy The Better

Now that it’s known that a faster metabolic rate is not the cause of a shorter lifespan, the popular narrative can be flipped on its head: running the human “machine” faster does not cause it to deteriorate quicker. Instead, the opposite is true.

As I’ve outlined in this article, energy is the driving force behind our health and all our bodily functions. From this bioenergetic view of health, it’s evident that the production of adequate amounts of energy is what allows for regeneration, rather than the deterioration and degeneration we see when energy production is impaired, such as in disease and aging.

Of course, this capacity for growth and regeneration isn’t compatible with a mechanical view of the human organism, further illustrating one of its many flaws.

 

As I’ve mentioned before, improving energy production is much easier said than done, as this process can be inhibited by various factors. I outline several of the key factors affecting energy production and usage, how they affect our health, and what you can do about them in my free health and energy balance mini-course, which you can sign up for below.

 

References

Aging, Metabolism, and Caloric Restriction

Live fast and die young,” “the flame that burns twice as bright burns half as long,” “don’t burn the candle at both ends.”

These phrases embody the idea that our resources are limited, and the faster we use them the sooner they, and we, are gone.

For a while, a similar idea prevailed in biology and medicine that suggested that we would live longer if we reduced the amount of energy we produced and used, as is explained in this quote:

“The idea that aging should be linked to energy expenditure has a long history that can be traced to the late 1800s and the industrial revolution. Machines that are run fast wear out more quickly, so the notion was born that humans and animals might experience similar fates: the faster they live (expressed as greater energy expenditure), the sooner they die.” (1)

The rate of living theory was born out of this mechanical view of biology and states that the greater an organism’s energy expenditure, the shorter it’s lifespan. It has since been expanded to suggest that aging, health, and lifespan are tied to energy expenditure.

This theory has been primarily supported by the evidence that animals with lower metabolic rates relative to their body mass have longer lifespans and that low-calorie diets extend lifespan by reducing the metabolic rate. But, it turns out it’s not quite that simple.

 

Aging and Metabolism

The concept that animals with higher metabolic rates have shorter lives isn’t particularly noteworthy. It’s now common knowledge that small animals, like mice, typically have high metabolic rates (relative to their size) and short lifespans, while large animals, like elephants, typically have low metabolic rates (relative to their size) and long lifespans.

This finding that species’ metabolic rates correlate with their lifespans corroborated the rate of living theory. However, while it was originally assumed that the metabolic rate was responsible for the rate of aging, we’ve since learned that there are other factors that explain this finding (1, 2).

The most notable of these factors is the composition of the cellular and mitochondrial phospholipid membranes (3, 4) [Note: while there’s substantial evidence that these “membranes” may not exist, the same principle applies to the composition of the non-membrane lipid structural components]. These membranes play a vital role in the production and usage of energy.

The fatty acids that make up these membranes vary in terms of their saturation. The more saturated the fatty acids are, the more structurally stable they are. Weaker, more unsaturated membranes are more susceptible to damage and have a higher permeability to protons and ions (3, 4, 5).

When the fatty acids in these membranes become damaged, they increase oxidative stress which damages all parts of our cells, including their protein structure, fatty acids, and DNA (3). This impairs energy production and requires energy for repair, making it doubly wasteful.

And, the increased permeability to protons and ions reduces the production of usable energy and increases the production of heat, which effectively reduces the efficiency of energy production (5). The increased permeability also increases the activity of Na+/K+ ATPase and proton pumps, which increases the energy demand (5) [Note: while there’s substantial evidence that these “pumps” may not exist, the same principle of an increased energy demand still applies].

Together, the differences in oxidative damage, wasting of energy, and efficiency of energy production due to differences in membrane saturation account for the differences in metabolic rates between species as well as the differences in aging and lifespan (3, 4).

In other words, species that have more saturated membranes are more energetically efficient and this results in slower aging.

And, what’s even more remarkable is that within species, where the membrane saturation is typically constant, those with the highest metabolic rates relative to their body weight actually live the longest (1, 2, 3). This supports the directly opposite conclusion of the rate of living theory: producing and using more energy slows aging and extends lifespan.

 

Aging and Caloric Restriction

Now, what about all those caloric restriction studies that show that eating less reduces the metabolic rate and increases lifespan?

While reducing caloric intake has been shown to reliably increase lifespan while also slowing the metabolic rate, there’s now considerable evidence that factors other than the reduction in metabolic rate are responsible for the life-extending effects of these calorie-restricting-diets.

Firstly, these caloric restriction studies are often performed by splitting the subjects into a caloric restriction group and a control group that eats ad-libitum (meaning they can eat as much as they want). This presents a problem because the subjects fed ad-libitum become overweight and are prone to the early onset of diseases and death, making them poor controls.

In fact, the supposed life-extending effects of caloric restriction are directly related to weight gain in the ad-libitum control groups (6). In other words, the less weight gain there is in the control group, the less life-extending effects are seen in the caloric restriction group. This suggests that the “life-extending effects” seen in the caloric restriction groups are simply due to life-shortening effects of the control groups.

Secondly, caloric restriction inherently reduces the consumption of amino acids that have been shown to reduce longevity and increase oxidative damage, including methionine, cysteine, and tryptophan. It’s been shown that the life-extending effects of caloric restriction can be entirely accounted for by the reduction of these amino acids in the diet (7, 8, 9, 10).

In other words, simply reducing the consumption of these amino acids without reducing caloric intake results in the same life-extending effects. These effects on aging can at least partially be accounted for by changes in membrane saturation, which I explained earlier is the primary determinant of lifespan between species (8).

Lastly, caloric restriction also inherently reduces the consumption of polyunsaturated fatty acids (PUFA). PUFA consumption is also directly related to membrane unsaturation, which accounts for many of its effects on aging, health, and lifespan. (I’ve written about PUFA’s negative effects on energy balance here and here.)

So, while it hasn’t been directly studied in this context, a reduction in PUFA consumption is likely another factor that accounts for the life-extending effects of caloric restriction.

All three of these factors are corroborated by other studies showing that reductions in the metabolic rate are not responsible for the life-extending effects of caloric restriction (11, 12) and that reductions in membrane unsaturation are (3, 13, 14, 15).

 

The More Energy The Better

Now that it’s known that a faster metabolic rate is not the cause of a shorter lifespan, the popular narrative can be flipped on its head: running the human “machine” faster does not cause it to deteriorate quicker. Instead, the opposite is true.

As I’ve outlined in this article, energy is the driving force behind our health and all our bodily functions. From this bioenergetic view of health, it’s evident that the production of adequate amounts of energy is what allows for regeneration, rather than the deterioration and degeneration we see when energy production is impaired, such as in disease and aging.

Of course, this capacity for growth and regeneration isn’t compatible with a mechanical view of the human organism, further illustrating one of its many flaws.

 

As I’ve mentioned before, improving energy production is much easier said than done, as this process can be inhibited by various factors. I outline several of the key factors affecting energy production and usage, how they affect our health, and what you can do about them in my free health and energy balance mini-course, which you can sign up for below.

 

References

Aging, Metabolism, and Caloric Restriction

Live fast and die young,” “the flame that burns twice as bright burns half as long,” “don’t burn the candle at both ends.”

These phrases embody the idea that our resources are limited, and the faster we use them the sooner they, and we, are gone.

For a while, a similar idea prevailed in biology and medicine that suggested that we would live longer if we reduced the amount of energy we produced and used, as is explained in this quote:

“The idea that aging should be linked to energy expenditure has a long history that can be traced to the late 1800s and the industrial revolution. Machines that are run fast wear out more quickly, so the notion was born that humans and animals might experience similar fates: the faster they live (expressed as greater energy expenditure), the sooner they die.” (1)

The rate of living theory was born out of this mechanical view of biology and states that the greater an organism’s energy expenditure, the shorter it’s lifespan. It has since been expanded to suggest that aging, health, and lifespan are tied to energy expenditure.

This theory has been primarily supported by the evidence that animals with lower metabolic rates relative to their body mass have longer lifespans and that low-calorie diets extend lifespan by reducing the metabolic rate. But, it turns out it’s not quite that simple.

 

Aging and Metabolism

The concept that animals with higher metabolic rates have shorter lives isn’t particularly noteworthy. It’s now common knowledge that small animals, like mice, typically have high metabolic rates (relative to their size) and short lifespans, while large animals, like elephants, typically have low metabolic rates (relative to their size) and long lifespans.

This finding that species’ metabolic rates correlate with their lifespans corroborated the rate of living theory. However, while it was originally assumed that the metabolic rate was responsible for the rate of aging, we’ve since learned that there are other factors that explain this finding (1, 2).

The most notable of these factors is the composition of the cellular and mitochondrial phospholipid membranes (3, 4) [Note: while there’s substantial evidence that these “membranes” may not exist, the same principle applies to the composition of the non-membrane lipid structural components]. These membranes play a vital role in the production and usage of energy.

The fatty acids that make up these membranes vary in terms of their saturation. The more saturated the fatty acids are, the more structurally stable they are. Weaker, more unsaturated membranes are more susceptible to damage and have a higher permeability to protons and ions (3, 4, 5).

When the fatty acids in these membranes become damaged, they increase oxidative stress which damages all parts of our cells, including their protein structure, fatty acids, and DNA (3). This impairs energy production and requires energy for repair, making it doubly wasteful.

And, the increased permeability to protons and ions reduces the production of usable energy and increases the production of heat, which effectively reduces the efficiency of energy production (5). The increased permeability also increases the activity of Na+/K+ ATPase and proton pumps, which increases the energy demand (5) [Note: while there’s substantial evidence that these “pumps” may not exist, the same principle of an increased energy demand still applies].

Together, the differences in oxidative damage, wasting of energy, and efficiency of energy production due to differences in membrane saturation account for the differences in metabolic rates between species as well as the differences in aging and lifespan (3, 4).

In other words, species that have more saturated membranes are more energetically efficient and this results in slower aging.

And, what’s even more remarkable is that within species, where the membrane saturation is typically constant, those with the highest metabolic rates relative to their body weight actually live the longest (1, 2, 3). This supports the directly opposite conclusion of the rate of living theory: producing and using more energy slows aging and extends lifespan.

 

Aging and Caloric Restriction

Now, what about all those caloric restriction studies that show that eating less reduces the metabolic rate and increases lifespan?

While reducing caloric intake has been shown to reliably increase lifespan while also slowing the metabolic rate, there’s now considerable evidence that factors other than the reduction in metabolic rate are responsible for the life-extending effects of these calorie-restricting-diets.

Firstly, these caloric restriction studies are often performed by splitting the subjects into a caloric restriction group and a control group that eats ad-libitum (meaning they can eat as much as they want). This presents a problem because the subjects fed ad-libitum become overweight and are prone to the early onset of diseases and death, making them poor controls.

In fact, the supposed life-extending effects of caloric restriction are directly related to weight gain in the ad-libitum control groups (6). In other words, the less weight gain there is in the control group, the less life-extending effects are seen in the caloric restriction group. This suggests that the “life-extending effects” seen in the caloric restriction groups are simply due to life-shortening effects of the control groups.

Secondly, caloric restriction inherently reduces the consumption of amino acids that have been shown to reduce longevity and increase oxidative damage, including methionine, cysteine, and tryptophan. It’s been shown that the life-extending effects of caloric restriction can be entirely accounted for by the reduction of these amino acids in the diet (7, 8, 9, 10).

In other words, simply reducing the consumption of these amino acids without reducing caloric intake results in the same life-extending effects. These effects on aging can at least partially be accounted for by changes in membrane saturation, which I explained earlier is the primary determinant of lifespan between species (8).

Lastly, caloric restriction also inherently reduces the consumption of polyunsaturated fatty acids (PUFA). PUFA consumption is also directly related to membrane unsaturation, which accounts for many of its effects on aging, health, and lifespan. (I’ve written about PUFA’s negative effects on energy balance here and here.)

So, while it hasn’t been directly studied in this context, a reduction in PUFA consumption is likely another factor that accounts for the life-extending effects of caloric restriction.

All three of these factors are corroborated by other studies showing that reductions in the metabolic rate are not responsible for the life-extending effects of caloric restriction (11, 12) and that reductions in membrane unsaturation are (3, 13, 14, 15).

 

The More Energy The Better

Now that it’s known that a faster metabolic rate is not the cause of a shorter lifespan, the popular narrative can be flipped on its head: running the human “machine” faster does not cause it to deteriorate quicker. Instead, the opposite is true.

As I’ve outlined in this article, energy is the driving force behind our health and all our bodily functions. From this bioenergetic view of health, it’s evident that the production of adequate amounts of energy is what allows for regeneration, rather than the deterioration and degeneration we see when energy production is impaired, such as in disease and aging.

Of course, this capacity for growth and regeneration isn’t compatible with a mechanical view of the human organism, further illustrating one of its many flaws.

 

As I’ve mentioned before, improving energy production is much easier said than done, as this process can be inhibited by various factors. I outline several of the key factors affecting energy production and usage, how they affect our health, and what you can do about them in my free health and energy balance mini-course, which you can sign up for below.

 

References

Aging, Metabolism, and Caloric Restriction

Live fast and die young,” “the flame that burns twice as bright burns half as long,” “don’t burn the candle at both ends.”

These phrases embody the idea that our resources are limited, and the faster we use them the sooner they, and we, are gone.

For a while, a similar idea prevailed in biology and medicine that suggested that we would live longer if we reduced the amount of energy we produced and used, as is explained in this quote:

“The idea that aging should be linked to energy expenditure has a long history that can be traced to the late 1800s and the industrial revolution. Machines that are run fast wear out more quickly, so the notion was born that humans and animals might experience similar fates: the faster they live (expressed as greater energy expenditure), the sooner they die.” (1)

The rate of living theory was born out of this mechanical view of biology and states that the greater an organism’s energy expenditure, the shorter it’s lifespan. It has since been expanded to suggest that aging, health, and lifespan are tied to energy expenditure.

This theory has been primarily supported by the evidence that animals with lower metabolic rates relative to their body mass have longer lifespans and that low-calorie diets extend lifespan by reducing the metabolic rate. But, it turns out it’s not quite that simple.

 

Aging and Metabolism

The concept that animals with higher metabolic rates have shorter lives isn’t particularly noteworthy. It’s now common knowledge that small animals, like mice, typically have high metabolic rates (relative to their size) and short lifespans, while large animals, like elephants, typically have low metabolic rates (relative to their size) and long lifespans.

This finding that species’ metabolic rates correlate with their lifespans corroborated the rate of living theory. However, while it was originally assumed that the metabolic rate was responsible for the rate of aging, we’ve since learned that there are other factors that explain this finding (1, 2).

The most notable of these factors is the composition of the cellular and mitochondrial phospholipid membranes (3, 4) [Note: while there’s substantial evidence that these “membranes” may not exist, the same principle applies to the composition of the non-membrane lipid structural components]. These membranes play a vital role in the production and usage of energy.

The fatty acids that make up these membranes vary in terms of their saturation. The more saturated the fatty acids are, the more structurally stable they are. Weaker, more unsaturated membranes are more susceptible to damage and have a higher permeability to protons and ions (3, 4, 5).

When the fatty acids in these membranes become damaged, they increase oxidative stress which damages all parts of our cells, including their protein structure, fatty acids, and DNA (3). This impairs energy production and requires energy for repair, making it doubly wasteful.

And, the increased permeability to protons and ions reduces the production of usable energy and increases the production of heat, which effectively reduces the efficiency of energy production (5). The increased permeability also increases the activity of Na+/K+ ATPase and proton pumps, which increases the energy demand (5) [Note: while there’s substantial evidence that these “pumps” may not exist, the same principle of an increased energy demand still applies].

Together, the differences in oxidative damage, wasting of energy, and efficiency of energy production due to differences in membrane saturation account for the differences in metabolic rates between species as well as the differences in aging and lifespan (3, 4).

In other words, species that have more saturated membranes are more energetically efficient and this results in slower aging.

And, what’s even more remarkable is that within species, where the membrane saturation is typically constant, those with the highest metabolic rates relative to their body weight actually live the longest (1, 2, 3). This supports the directly opposite conclusion of the rate of living theory: producing and using more energy slows aging and extends lifespan.

 

Aging and Caloric Restriction

Now, what about all those caloric restriction studies that show that eating less reduces the metabolic rate and increases lifespan?

While reducing caloric intake has been shown to reliably increase lifespan while also slowing the metabolic rate, there’s now considerable evidence that factors other than the reduction in metabolic rate are responsible for the life-extending effects of these calorie-restricting-diets.

Firstly, these caloric restriction studies are often performed by splitting the subjects into a caloric restriction group and a control group that eats ad-libitum (meaning they can eat as much as they want). This presents a problem because the subjects fed ad-libitum become overweight and are prone to the early onset of diseases and death, making them poor controls.

In fact, the supposed life-extending effects of caloric restriction are directly related to weight gain in the ad-libitum control groups (6). In other words, the less weight gain there is in the control group, the less life-extending effects are seen in the caloric restriction group. This suggests that the “life-extending effects” seen in the caloric restriction groups are simply due to life-shortening effects of the control groups.

Secondly, caloric restriction inherently reduces the consumption of amino acids that have been shown to reduce longevity and increase oxidative damage, including methionine, cysteine, and tryptophan. It’s been shown that the life-extending effects of caloric restriction can be entirely accounted for by the reduction of these amino acids in the diet (7, 8, 9, 10).

In other words, simply reducing the consumption of these amino acids without reducing caloric intake results in the same life-extending effects. These effects on aging can at least partially be accounted for by changes in membrane saturation, which I explained earlier is the primary determinant of lifespan between species (8).

Lastly, caloric restriction also inherently reduces the consumption of polyunsaturated fatty acids (PUFA). PUFA consumption is also directly related to membrane unsaturation, which accounts for many of its effects on aging, health, and lifespan. (I’ve written about PUFA’s negative effects on energy balance here and here.)

So, while it hasn’t been directly studied in this context, a reduction in PUFA consumption is likely another factor that accounts for the life-extending effects of caloric restriction.

All three of these factors are corroborated by other studies showing that reductions in the metabolic rate are not responsible for the life-extending effects of caloric restriction (11, 12) and that reductions in membrane unsaturation are (3, 13, 14, 15).

 

The More Energy The Better

Now that it’s known that a faster metabolic rate is not the cause of a shorter lifespan, the popular narrative can be flipped on its head: running the human “machine” faster does not cause it to deteriorate quicker. Instead, the opposite is true.

As I’ve outlined in this article, energy is the driving force behind our health and all our bodily functions. From this bioenergetic view of health, it’s evident that the production of adequate amounts of energy is what allows for regeneration, rather than the deterioration and degeneration we see when energy production is impaired, such as in disease and aging.

Of course, this capacity for growth and regeneration isn’t compatible with a mechanical view of the human organism, further illustrating one of its many flaws.

 

As I’ve mentioned before, improving energy production is much easier said than done, as this process can be inhibited by various factors. I outline several of the key factors affecting energy production and usage, how they affect our health, and what you can do about them in my free health and energy balance mini-course, which you can sign up for below.

 

References

Aging, Metabolism, and Caloric Restriction

Live fast and die young,” “the flame that burns twice as bright burns half as long,” “don’t burn the candle at both ends.”

These phrases embody the idea that our resources are limited, and the faster we use them the sooner they, and we, are gone.

For a while, a similar idea prevailed in biology and medicine that suggested that we would live longer if we reduced the amount of energy we produced and used, as is explained in this quote:

“The idea that aging should be linked to energy expenditure has a long history that can be traced to the late 1800s and the industrial revolution. Machines that are run fast wear out more quickly, so the notion was born that humans and animals might experience similar fates: the faster they live (expressed as greater energy expenditure), the sooner they die.” (1)

The rate of living theory was born out of this mechanical view of biology and states that the greater an organism’s energy expenditure, the shorter it’s lifespan. It has since been expanded to suggest that aging, health, and lifespan are tied to energy expenditure.

This theory has been primarily supported by the evidence that animals with lower metabolic rates relative to their body mass have longer lifespans and that low-calorie diets extend lifespan by reducing the metabolic rate. But, it turns out it’s not quite that simple.

 

Aging and Metabolism

The concept that animals with higher metabolic rates have shorter lives isn’t particularly noteworthy. It’s now common knowledge that small animals, like mice, typically have high metabolic rates (relative to their size) and short lifespans, while large animals, like elephants, typically have low metabolic rates (relative to their size) and long lifespans.

This finding that species’ metabolic rates correlate with their lifespans corroborated the rate of living theory. However, while it was originally assumed that the metabolic rate was responsible for the rate of aging, we’ve since learned that there are other factors that explain this finding (1, 2).

The most notable of these factors is the composition of the cellular and mitochondrial phospholipid membranes (3, 4) [Note: while there’s substantial evidence that these “membranes” may not exist, the same principle applies to the composition of the non-membrane lipid structural components]. These membranes play a vital role in the production and usage of energy.

The fatty acids that make up these membranes vary in terms of their saturation. The more saturated the fatty acids are, the more structurally stable they are. Weaker, more unsaturated membranes are more susceptible to damage and have a higher permeability to protons and ions (3, 4, 5).

When the fatty acids in these membranes become damaged, they increase oxidative stress which damages all parts of our cells, including their protein structure, fatty acids, and DNA (3). This impairs energy production and requires energy for repair, making it doubly wasteful.

And, the increased permeability to protons and ions reduces the production of usable energy and increases the production of heat, which effectively reduces the efficiency of energy production (5). The increased permeability also increases the activity of Na+/K+ ATPase and proton pumps, which increases the energy demand (5) [Note: while there’s substantial evidence that these “pumps” may not exist, the same principle of an increased energy demand still applies].

Together, the differences in oxidative damage, wasting of energy, and efficiency of energy production due to differences in membrane saturation account for the differences in metabolic rates between species as well as the differences in aging and lifespan (3, 4).

In other words, species that have more saturated membranes are more energetically efficient and this results in slower aging.

And, what’s even more remarkable is that within species, where the membrane saturation is typically constant, those with the highest metabolic rates relative to their body weight actually live the longest (1, 2, 3). This supports the directly opposite conclusion of the rate of living theory: producing and using more energy slows aging and extends lifespan.

 

Aging and Caloric Restriction

Now, what about all those caloric restriction studies that show that eating less reduces the metabolic rate and increases lifespan?

While reducing caloric intake has been shown to reliably increase lifespan while also slowing the metabolic rate, there’s now considerable evidence that factors other than the reduction in metabolic rate are responsible for the life-extending effects of these calorie-restricting-diets.

Firstly, these caloric restriction studies are often performed by splitting the subjects into a caloric restriction group and a control group that eats ad-libitum (meaning they can eat as much as they want). This presents a problem because the subjects fed ad-libitum become overweight and are prone to the early onset of diseases and death, making them poor controls.

In fact, the supposed life-extending effects of caloric restriction are directly related to weight gain in the ad-libitum control groups (6). In other words, the less weight gain there is in the control group, the less life-extending effects are seen in the caloric restriction group. This suggests that the “life-extending effects” seen in the caloric restriction groups are simply due to life-shortening effects of the control groups.

Secondly, caloric restriction inherently reduces the consumption of amino acids that have been shown to reduce longevity and increase oxidative damage, including methionine, cysteine, and tryptophan. It’s been shown that the life-extending effects of caloric restriction can be entirely accounted for by the reduction of these amino acids in the diet (7, 8, 9, 10).

In other words, simply reducing the consumption of these amino acids without reducing caloric intake results in the same life-extending effects. These effects on aging can at least partially be accounted for by changes in membrane saturation, which I explained earlier is the primary determinant of lifespan between species (8).

Lastly, caloric restriction also inherently reduces the consumption of polyunsaturated fatty acids (PUFA). PUFA consumption is also directly related to membrane unsaturation, which accounts for many of its effects on aging, health, and lifespan. (I’ve written about PUFA’s negative effects on energy balance here and here.)

So, while it hasn’t been directly studied in this context, a reduction in PUFA consumption is likely another factor that accounts for the life-extending effects of caloric restriction.

All three of these factors are corroborated by other studies showing that reductions in the metabolic rate are not responsible for the life-extending effects of caloric restriction (11, 12) and that reductions in membrane unsaturation are (3, 13, 14, 15).

 

The More Energy The Better

Now that it’s known that a faster metabolic rate is not the cause of a shorter lifespan, the popular narrative can be flipped on its head: running the human “machine” faster does not cause it to deteriorate quicker. Instead, the opposite is true.

As I’ve outlined in this article, energy is the driving force behind our health and all our bodily functions. From this bioenergetic view of health, it’s evident that the production of adequate amounts of energy is what allows for regeneration, rather than the deterioration and degeneration we see when energy production is impaired, such as in disease and aging.

Of course, this capacity for growth and regeneration isn’t compatible with a mechanical view of the human organism, further illustrating one of its many flaws.

 

As I’ve mentioned before, improving energy production is much easier said than done, as this process can be inhibited by various factors. I outline several of the key factors affecting energy production and usage, how they affect our health, and what you can do about them in my free health and energy balance mini-course, which you can sign up for below.

 

References

Aging, Metabolism, and Caloric Restriction

Live fast and die young,” “the flame that burns twice as bright burns half as long,” “don’t burn the candle at both ends.”

These phrases embody the idea that our resources are limited, and the faster we use them the sooner they, and we, are gone.

For a while, a similar idea prevailed in biology and medicine that suggested that we would live longer if we reduced the amount of energy we produced and used, as is explained in this quote:

“The idea that aging should be linked to energy expenditure has a long history that can be traced to the late 1800s and the industrial revolution. Machines that are run fast wear out more quickly, so the notion was born that humans and animals might experience similar fates: the faster they live (expressed as greater energy expenditure), the sooner they die.” (1)

The rate of living theory was born out of this mechanical view of biology and states that the greater an organism’s energy expenditure, the shorter it’s lifespan. It has since been expanded to suggest that aging, health, and lifespan are tied to energy expenditure.

This theory has been primarily supported by the evidence that animals with lower metabolic rates relative to their body mass have longer lifespans and that low-calorie diets extend lifespan by reducing the metabolic rate. But, it turns out it’s not quite that simple.

 

Aging and Metabolism

The concept that animals with higher metabolic rates have shorter lives isn’t particularly noteworthy. It’s now common knowledge that small animals, like mice, typically have high metabolic rates (relative to their size) and short lifespans, while large animals, like elephants, typically have low metabolic rates (relative to their size) and long lifespans.

This finding that species’ metabolic rates correlate with their lifespans corroborated the rate of living theory. However, while it was originally assumed that the metabolic rate was responsible for the rate of aging, we’ve since learned that there are other factors that explain this finding (1, 2).

The most notable of these factors is the composition of the cellular and mitochondrial phospholipid membranes (3, 4) [Note: while there’s substantial evidence that these “membranes” may not exist, the same principle applies to the composition of the non-membrane lipid structural components]. These membranes play a vital role in the production and usage of energy.

The fatty acids that make up these membranes vary in terms of their saturation. The more saturated the fatty acids are, the more structurally stable they are. Weaker, more unsaturated membranes are more susceptible to damage and have a higher permeability to protons and ions (3, 4, 5).

When the fatty acids in these membranes become damaged, they increase oxidative stress which damages all parts of our cells, including their protein structure, fatty acids, and DNA (3). This impairs energy production and requires energy for repair, making it doubly wasteful.

And, the increased permeability to protons and ions reduces the production of usable energy and increases the production of heat, which effectively reduces the efficiency of energy production (5). The increased permeability also increases the activity of Na+/K+ ATPase and proton pumps, which increases the energy demand (5) [Note: while there’s substantial evidence that these “pumps” may not exist, the same principle of an increased energy demand still applies].

Together, the differences in oxidative damage, wasting of energy, and efficiency of energy production due to differences in membrane saturation account for the differences in metabolic rates between species as well as the differences in aging and lifespan (3, 4).

In other words, species that have more saturated membranes are more energetically efficient and this results in slower aging.

And, what’s even more remarkable is that within species, where the membrane saturation is typically constant, those with the highest metabolic rates relative to their body weight actually live the longest (1, 2, 3). This supports the directly opposite conclusion of the rate of living theory: producing and using more energy slows aging and extends lifespan.

 

Aging and Caloric Restriction

Now, what about all those caloric restriction studies that show that eating less reduces the metabolic rate and increases lifespan?

While reducing caloric intake has been shown to reliably increase lifespan while also slowing the metabolic rate, there’s now considerable evidence that factors other than the reduction in metabolic rate are responsible for the life-extending effects of these calorie-restricting-diets.

Firstly, these caloric restriction studies are often performed by splitting the subjects into a caloric restriction group and a control group that eats ad-libitum (meaning they can eat as much as they want). This presents a problem because the subjects fed ad-libitum become overweight and are prone to the early onset of diseases and death, making them poor controls.

In fact, the supposed life-extending effects of caloric restriction are directly related to weight gain in the ad-libitum control groups (6). In other words, the less weight gain there is in the control group, the less life-extending effects are seen in the caloric restriction group. This suggests that the “life-extending effects” seen in the caloric restriction groups are simply due to life-shortening effects of the control groups.

Secondly, caloric restriction inherently reduces the consumption of amino acids that have been shown to reduce longevity and increase oxidative damage, including methionine, cysteine, and tryptophan. It’s been shown that the life-extending effects of caloric restriction can be entirely accounted for by the reduction of these amino acids in the diet (7, 8, 9, 10).

In other words, simply reducing the consumption of these amino acids without reducing caloric intake results in the same life-extending effects. These effects on aging can at least partially be accounted for by changes in membrane saturation, which I explained earlier is the primary determinant of lifespan between species (8).

Lastly, caloric restriction also inherently reduces the consumption of polyunsaturated fatty acids (PUFA). PUFA consumption is also directly related to membrane unsaturation, which accounts for many of its effects on aging, health, and lifespan. (I’ve written about PUFA’s negative effects on energy balance here and here.)

So, while it hasn’t been directly studied in this context, a reduction in PUFA consumption is likely another factor that accounts for the life-extending effects of caloric restriction.

All three of these factors are corroborated by other studies showing that reductions in the metabolic rate are not responsible for the life-extending effects of caloric restriction (11, 12) and that reductions in membrane unsaturation are (3, 13, 14, 15).

 

The More Energy The Better

Now that it’s known that a faster metabolic rate is not the cause of a shorter lifespan, the popular narrative can be flipped on its head: running the human “machine” faster does not cause it to deteriorate quicker. Instead, the opposite is true.

As I’ve outlined in this article, energy is the driving force behind our health and all our bodily functions. From this bioenergetic view of health, it’s evident that the production of adequate amounts of energy is what allows for regeneration, rather than the deterioration and degeneration we see when energy production is impaired, such as in disease and aging.

Of course, this capacity for growth and regeneration isn’t compatible with a mechanical view of the human organism, further illustrating one of its many flaws.

 

As I’ve mentioned before, improving energy production is much easier said than done, as this process can be inhibited by various factors. I outline several of the key factors affecting energy production and usage, how they affect our health, and what you can do about them in my free health and energy balance mini-course, which you can sign up for below.

 

References

Carbs vs. Fats: Which is the Better Fuel?

It’s time for the age-old debate: carbs vs. fats.

There’s a ton of disagreement on this topic with poorly supported arguments on both sides.

Most of the current recommendations are now favoring the low-carb “fat-burning approach.” This is “supported” by all sorts of nonsense, such as that “carbohydrates aren’t essential to our diets,” “carbohydrates cause blood sugar dysregulation,” “burning fat leads to fat loss,” and “our ancestors didn’t eat carbohydrates,” among others.

While I’m tempted to go through each of these ridiculous arguments right now and explain why they aren’t at all valid, I’ll have to save that for another time.

There are many differences between the effects of consuming carbohydrates and fats that can be explored, including their interactions with various hormones, effects on blood sugar, distribution throughout the body, and many other differences, as well as the variations between the different types of carbohydrates and fats. However, while these are important topics, the answer to this debate becomes quite clear when you consider it from a bioenergetic point of view.

So in this article, I’m going to focus solely on the usage of carbs and fats as fuel to produce energy. There’s quite a bit of misinformation out there about “fat-burning” versus “sugar-burning” and their effects on energy production and mitochondrial function, and I’m going to clear that up.

In order to do that, I’m going to dive into the biochemistry of carbohydrate and fat oxidation. If you want a general overview of this topic without all the biochemistry, check out this article.

Also, I’d like to preface this article by pointing out that we’re never burning only carbs or only fats, there’s always some combination of these fuels being used, but which fuel we predominantly use does make a difference.

Carbohydrate Oxidation vs. Fat Oxidation

When considering the oxidation of carbohydrates and fats through mitochondrial respiration, a majority of the process is the same – once each of these substrates is converted to acetyl-CoA (ACoA), the rest is identical.

But, there are several important differences between carbohydrate and fat oxidation that occur before they become ACoA. While these differences may seem small, they’re responsible for the significantly increased efficiency of glucose oxidation over fat oxidation.

The oxidation of carbohydrates begins with glycolysis, where glucose is eventually converted into pyruvate and then either lactate or ACoA. For each molecule of ACoA that’s produced through this process, 1 net molecule of ATP, 2 molecules of NADH, and 1 molecule of carbon dioxide (CO2) are produced.

The oxidation of fats, on the other hand, begins with beta-oxidation, where the fatty acid is converted to ACoA. For each molecule of ACoA that’s produced through this process, on average, 1 molecule of NADH and 1 molecule of FADH2 are produced.

There are two key differences here that have significant effects on mitochondrial respiration:

  • The additional CO2 production in glucose oxidation, and
  • The replacement of 1 molecule of NADH with 1 molecule of FADH2 in fat oxidation

Let’s explore each of these differences more closely.

Carbon Dioxide, Simply A Waste Product?

CO2 is often considered a waste product of mitochondrial respiration, but this couldn’t be farther from the truth. In fact, CO2 is one of the most protective compounds in our bodies.

The oxidation of carbohydrates produces 50% more CO2 than the oxidation of fat, which is a major difference that has a dramatic effect on the efficiency of mitochondrial respiration for a couple reasons.

For one, CO2 production is vital for the proper oxygenation of our cells.

Our cells require oxygen (O2) for efficient energy production, as oxygen acts as the final electron acceptor in the electron transport chain. In order to be delivered to our cells from our lungs, oxygen is carried through our blood in our red blood cells via a protein called hemoglobin, which is able to bind with both O2 and CO2.

In low CO2 environments, hemoglobin releases CO2 and binds with O2, which is called the Haldane effect. This allows our red blood cells to drop off CO2 and pick up O2 at our lungs. In high CO2 (or acidic) environments, hemoglobin releases O2 and binds with CO2, which is called the Bohr effect. This allows our red blood cells to offload O2 at our tissues, where it’s needed to produce energy.

So, when our cells produce more CO2, as they do from glucose oxidation, our tissues receive more O2 (1). When our cells don’t produce enough CO2, preventing enough oxygen from entering the cell, glucose is converted to lactate as opposed to ACoA and the function of the electron transport chain is impaired, drastically inhibiting energy production and increasing reactive oxygen species production (2, 3, 4, 5).

(Note: CO2 is also a potent vasodilator, which further increases oxygen delivery to our tissues.)

Second, CO2 acts as a powerful protector against reactive oxygen species (ROS), reactive nitrogen species (RNS), and lipid peroxidation (6, 7, 8).

These compounds all damage our cells and inhibit energy production, making protection against these compounds extremely important.

Considering these factors, the increased CO2 production as a result of glucose oxidation results in significantly more efficient mitochondrial respiration than fat oxidation.

NADH vs. FADH2

NADH and FADH2 are both electron carriers that donate electrons at the electron transport chain (ETC), allowing for the production of ATP. NADH donates electrons at complex I of the ETC, whereas FADH2 donates electrons at complex II, and these complexes compete for the same electron acceptor, ubiquinone.

Glucose oxidation produces around 25% more NADH and half as much FADH2 as fat oxidation. Together, this leads to a ratio of FADH2 to NADH that is around 2.5 times lower than that of fat oxidation (9, 10). This difference has substantial effects that extend throughout the processes of mitochondrial respiration.

Because FADH2 donates electrons at complex II, downstream of complex I, it reduces the amount of ubiquinone available to accept electrons at complex I, leading to a buildup of electrons at complex I. This results in two major problems.

For one, this increases the electron leakage at complex I, which increases the production of ROS, specifically superoxide (9, 10, 11).

ROS are a major cause of cellular oxidative stress, and as I’ve already mentioned, damage the cell and inhibit energy production.

Second, the buildup of electrons at complex I reduces the donation of electrons by NADH, leading to a buildup of NADH and a decrease in the ratio of NAD+ to NADH (9, 10, 11, 12).

The ratio of NAD+ to NADH is a major controller of mitochondrial respiration and is also tied to aging, cancer, diabetes, neurodegeneration, and many other diseases (13, 14, 15).

A low NAD+/NADH ratio inhibits isocitrate dehydrogenase (IDH), the rate-limiting step of the TCA cycle (aka Krebs or citric acid cycle). This slows down the activity of the TCA cycle and leads to a buildup of citrate, which inhibits phosphofructokinase (PFK), the rate-limiting step of glycolysis, while also causing a buildup of ACoA (11).

The low NAD+/NADH ratio also inhibits pyruvate dehydrogenase (PDH), the rate-limiting-step that connects glycolysis to the TCA cycle, and the buildup of ACoA further inhibits PDH (11). This directs pyruvate towards lactate rather than ACoA.

The inhibition of glucose oxidation by fat oxidation through these mechanisms is a feature of the Randle cycle and is responsible for the insulin resistance seen in response to high-fat meals and diets (16). This is, of course, an adaptive response to using fat for fuel and is not a problem per se.

However, in this state, glycolysis is inhibited to a lesser degree than PDH, resulting in an increased production of lactate which can cause problems of its own (11, 17, 18). And, the decrease in the NAD+/NADH ratio still reduces the activity of the TCA cycle through the inhibition of IDH, which slows energy production.

Overall, fat oxidation drastically reduces the efficiency of energy production, causing much less energy to be produced while increasing ROS production, which has a damaging and destabilizing effect (11, 19).

What Does This Mean For Our Health?

Fat is our backup fuel, reserved for times when carbohydrates aren’t available, such as in a state of famine or starvation. This is evidenced by the fact that the presence of carbs, or lack thereof, is what determines the relative amount of fat oxidation (20). So, when relying on fat for energy production, it’s no wonder why there are mechanisms in place to slow our energy production – it allows us to survive longer during these sorts of stressful times.

However, it’s clear that for our brain, our most energy-intensive organ, fats simply cannot efficiently provide enough energy for proper function, which is why sugars or ketones are required as fuel. Many of our other tissues, however, can still function using solely fat as fuel.

But is this ideal for health?

As I postulated in this article, energy lies at the foundation of our health and allows our bodies to properly function. And, energy deficiencies underlie virtually all the chronic health conditions we’re seeing in epidemic proportions, as well as fat gain.

Although, it’s worth pointing out that fat oxidation isn’t the most common cause of energy deficiencies.

Energy deficiencies are most commonly a result of the various factors that impair the oxidation of glucose, like PUFA or endotoxin, even in the context of adequate glucose availability. In this context, fatty acid oxidation is also partially inhibited due to the presence of high amounts of glucose and insulin.

This results in the inhibition of both glucose and fat oxidation, leading to severe energy deficiencies and extreme stress.

This is why it’s common for health to improve when switching to a low-carb or ketogenic diet, at least at first. By reducing the amount of glucose available, insulin is suppressed and fatty acid oxidation and ketone production can increase to supply enough energy to improve function.

While this is a much better situation than when both glucose and fat oxidation are inhibited, it’s still not ideal. Considering that carbohydrate oxidation provides more energy more efficiently, and energy is the driving force behind our health, providing as much energy as we can from carbohydrate oxidation is probably ideal.

But, this doesn’t mean we need to avoid fat altogether. Fat serves many purposes in our body beyond its use as a fuel source, such as its function as a structural component of our cells and its antimicrobial effects. While we can produce fat endogenously to fill these roles without consuming it, this doesn’t mean that we need to eliminate fat from our diet as long as carbohydrates are our primary fuel source.

References

Carbs vs. Fats: Which is the Better Fuel?

It’s time for the age-old debate: carbs vs. fats.

There’s a ton of disagreement on this topic with poorly supported arguments on both sides.

Most of the current recommendations are now favoring the low-carb “fat-burning approach.” This is “supported” by all sorts of nonsense, such as that “carbohydrates aren’t essential to our diets,” “carbohydrates cause blood sugar dysregulation,” “burning fat leads to fat loss,” and “our ancestors didn’t eat carbohydrates,” among others.

While I’m tempted to go through each of these ridiculous arguments right now and explain why they aren’t at all valid, I’ll have to save that for another time.

There are many differences between the effects of consuming carbohydrates and fats that can be explored, including their interactions with various hormones, effects on blood sugar, distribution throughout the body, and many other differences, as well as the variations between the different types of carbohydrates and fats. However, while these are important topics, the answer to this debate becomes quite clear when you consider it from a bioenergetic point of view.

So in this article, I’m going to focus solely on the usage of carbs and fats as fuel to produce energy. There’s quite a bit of misinformation out there about “fat-burning” versus “sugar-burning” and their effects on energy production and mitochondrial function, and I’m going to clear that up.

In order to do that, I’m going to dive into the biochemistry of carbohydrate and fat oxidation. If you want a general overview of this topic without all the biochemistry, check out this article.

Also, I’d like to preface this article by pointing out that we’re never burning only carbs or only fats, there’s always some combination of these fuels being used, but which fuel we predominantly use does make a difference.

Carbohydrate Oxidation vs. Fat Oxidation

When considering the oxidation of carbohydrates and fats through mitochondrial respiration, a majority of the process is the same – once each of these substrates is converted to acetyl-CoA (ACoA), the rest is identical.

But, there are several important differences between carbohydrate and fat oxidation that occur before they become ACoA. While these differences may seem small, they’re responsible for the significantly increased efficiency of glucose oxidation over fat oxidation.

The oxidation of carbohydrates begins with glycolysis, where glucose is eventually converted into pyruvate and then either lactate or ACoA. For each molecule of ACoA that’s produced through this process, 1 net molecule of ATP, 2 molecules of NADH, and 1 molecule of carbon dioxide (CO2) are produced.

The oxidation of fats, on the other hand, begins with beta-oxidation, where the fatty acid is converted to ACoA. For each molecule of ACoA that’s produced through this process, on average, 1 molecule of NADH and 1 molecule of FADH2 are produced.

There are two key differences here that have significant effects on mitochondrial respiration:

  • The additional CO2 production in glucose oxidation, and
  • The replacement of 1 molecule of NADH with 1 molecule of FADH2 in fat oxidation

Let’s explore each of these differences more closely.

Carbon Dioxide, Simply A Waste Product?

CO2 is often considered a waste product of mitochondrial respiration, but this couldn’t be farther from the truth. In fact, CO2 is one of the most protective compounds in our bodies.

The oxidation of carbohydrates produces 50% more CO2 than the oxidation of fat, which is a major difference that has a dramatic effect on the efficiency of mitochondrial respiration for a couple reasons.

For one, CO2 production is vital for the proper oxygenation of our cells.

Our cells require oxygen (O2) for efficient energy production, as oxygen acts as the final electron acceptor in the electron transport chain. In order to be delivered to our cells from our lungs, oxygen is carried through our blood in our red blood cells via a protein called hemoglobin, which is able to bind with both O2 and CO2.

In low CO2 environments, hemoglobin releases CO2 and binds with O2, which is called the Haldane effect. This allows our red blood cells to drop off CO2 and pick up O2 at our lungs. In high CO2 (or acidic) environments, hemoglobin releases O2 and binds with CO2, which is called the Bohr effect. This allows our red blood cells to offload O2 at our tissues, where it’s needed to produce energy.

So, when our cells produce more CO2, as they do from glucose oxidation, our tissues receive more O2 (1). When our cells don’t produce enough CO2, preventing enough oxygen from entering the cell, glucose is converted to lactate as opposed to ACoA and the function of the electron transport chain is impaired, drastically inhibiting energy production and increasing reactive oxygen species production (2, 3, 4, 5).

(Note: CO2 is also a potent vasodilator, which further increases oxygen delivery to our tissues.)

Second, CO2 acts as a powerful protector against reactive oxygen species (ROS), reactive nitrogen species (RNS), and lipid peroxidation (6, 7, 8).

These compounds all damage our cells and inhibit energy production, making protection against these compounds extremely important.

Considering these factors, the increased CO2 production as a result of glucose oxidation results in significantly more efficient mitochondrial respiration than fat oxidation.

NADH vs. FADH2

NADH and FADH2 are both electron carriers that donate electrons at the electron transport chain (ETC), allowing for the production of ATP. NADH donates electrons at complex I of the ETC, whereas FADH2 donates electrons at complex II, and these complexes compete for the same electron acceptor, ubiquinone.

Glucose oxidation produces around 25% more NADH and half as much FADH2 as fat oxidation. Together, this leads to a ratio of FADH2 to NADH that is around 2.5 times lower than that of fat oxidation (9, 10). This difference has substantial effects that extend throughout the processes of mitochondrial respiration.

Because FADH2 donates electrons at complex II, downstream of complex I, it reduces the amount of ubiquinone available to accept electrons at complex I, leading to a buildup of electrons at complex I. This results in two major problems.

For one, this increases the electron leakage at complex I, which increases the production of ROS, specifically superoxide (9, 10, 11).

ROS are a major cause of cellular oxidative stress, and as I’ve already mentioned, damage the cell and inhibit energy production.

Second, the buildup of electrons at complex I reduces the donation of electrons by NADH, leading to a buildup of NADH and a decrease in the ratio of NAD+ to NADH (9, 10, 11, 12).

The ratio of NAD+ to NADH is a major controller of mitochondrial respiration and is also tied to aging, cancer, diabetes, neurodegeneration, and many other diseases (13, 14, 15).

A low NAD+/NADH ratio inhibits isocitrate dehydrogenase (IDH), the rate-limiting step of the TCA cycle (aka Krebs or citric acid cycle). This slows down the activity of the TCA cycle and leads to a buildup of citrate, which inhibits phosphofructokinase (PFK), the rate-limiting step of glycolysis, while also causing a buildup of ACoA (11).

The low NAD+/NADH ratio also inhibits pyruvate dehydrogenase (PDH), the rate-limiting-step that connects glycolysis to the TCA cycle, and the buildup of ACoA further inhibits PDH (11). This directs pyruvate towards lactate rather than ACoA.

The inhibition of glucose oxidation by fat oxidation through these mechanisms is a feature of the Randle cycle and is responsible for the insulin resistance seen in response to high-fat meals and diets (16). This is, of course, an adaptive response to using fat for fuel and is not a problem per se.

However, in this state, glycolysis is inhibited to a lesser degree than PDH, resulting in an increased production of lactate which can cause problems of its own (11, 17, 18). And, the decrease in the NAD+/NADH ratio still reduces the activity of the TCA cycle through the inhibition of IDH, which slows energy production.

Overall, fat oxidation drastically reduces the efficiency of energy production, causing much less energy to be produced while increasing ROS production, which has a damaging and destabilizing effect (11, 19).

What Does This Mean For Our Health?

Fat is our backup fuel, reserved for times when carbohydrates aren’t available, such as in a state of famine or starvation. This is evidenced by the fact that the presence of carbs, or lack thereof, is what determines the relative amount of fat oxidation (20). So, when relying on fat for energy production, it’s no wonder why there are mechanisms in place to slow our energy production – it allows us to survive longer during these sorts of stressful times.

However, it’s clear that for our brain, our most energy-intensive organ, fats simply cannot efficiently provide enough energy for proper function, which is why sugars or ketones are required as fuel. Many of our other tissues, however, can still function using solely fat as fuel.

But is this ideal for health?

As I postulated in this article, energy lies at the foundation of our health and allows our bodies to properly function. And, energy deficiencies underlie virtually all the chronic health conditions we’re seeing in epidemic proportions, as well as fat gain.

Although, it’s worth pointing out that fat oxidation isn’t the most common cause of energy deficiencies.

Energy deficiencies are most commonly a result of the various factors that impair the oxidation of glucose, like PUFA or endotoxin, even in the context of adequate glucose availability. In this context, fatty acid oxidation is also partially inhibited due to the presence of high amounts of glucose and insulin.

This results in the inhibition of both glucose and fat oxidation, leading to severe energy deficiencies and extreme stress.

This is why it’s common for health to improve when switching to a low-carb or ketogenic diet, at least at first. By reducing the amount of glucose available, insulin is suppressed and fatty acid oxidation and ketone production can increase to supply enough energy to improve function.

While this is a much better situation than when both glucose and fat oxidation are inhibited, it’s still not ideal. Considering that carbohydrate oxidation provides more energy more efficiently, and energy is the driving force behind our health, providing as much energy as we can from carbohydrate oxidation is probably ideal.

But, this doesn’t mean we need to avoid fat altogether. Fat serves many purposes in our body beyond its use as a fuel source, such as its function as a structural component of our cells and its antimicrobial effects. While we can produce fat endogenously to fill these roles without consuming it, this doesn’t mean that we need to eliminate fat from our diet as long as carbohydrates are our primary fuel source.

References

Carbs vs. Fats: Which is the Better Fuel?

It’s time for the age-old debate: carbs vs. fats.

There’s a ton of disagreement on this topic with poorly supported arguments on both sides.

Most of the current recommendations are now favoring the low-carb “fat-burning approach.” This is “supported” by all sorts of nonsense, such as that “carbohydrates aren’t essential to our diets,” “carbohydrates cause blood sugar dysregulation,” “burning fat leads to fat loss,” and “our ancestors didn’t eat carbohydrates,” among others.

While I’m tempted to go through each of these ridiculous arguments right now and explain why they aren’t at all valid, I’ll have to save that for another time.

There are many differences between the effects of consuming carbohydrates and fats that can be explored, including their interactions with various hormones, effects on blood sugar, distribution throughout the body, and many other differences, as well as the variations between the different types of carbohydrates and fats. However, while these are important topics, the answer to this debate becomes quite clear when you consider it from a bioenergetic point of view.

So in this article, I’m going to focus solely on the usage of carbs and fats as fuel to produce energy. There’s quite a bit of misinformation out there about “fat-burning” versus “sugar-burning” and their effects on energy production and mitochondrial function, and I’m going to clear that up.

In order to do that, I’m going to dive into the biochemistry of carbohydrate and fat oxidation. If you want a general overview of this topic without all the biochemistry, check out this article.

Also, I’d like to preface this article by pointing out that we’re never burning only carbs or only fats, there’s always some combination of these fuels being used, but which fuel we predominantly use does make a difference.

Carbohydrate Oxidation vs. Fat Oxidation

When considering the oxidation of carbohydrates and fats through mitochondrial respiration, a majority of the process is the same – once each of these substrates is converted to acetyl-CoA (ACoA), the rest is identical.

But, there are several important differences between carbohydrate and fat oxidation that occur before they become ACoA. While these differences may seem small, they’re responsible for the significantly increased efficiency of glucose oxidation over fat oxidation.

The oxidation of carbohydrates begins with glycolysis, where glucose is eventually converted into pyruvate and then either lactate or ACoA. For each molecule of ACoA that’s produced through this process, 1 net molecule of ATP, 2 molecules of NADH, and 1 molecule of carbon dioxide (CO2) are produced.

The oxidation of fats, on the other hand, begins with beta-oxidation, where the fatty acid is converted to ACoA. For each molecule of ACoA that’s produced through this process, on average, 1 molecule of NADH and 1 molecule of FADH2 are produced.

There are two key differences here that have significant effects on mitochondrial respiration:

  • The additional CO2 production in glucose oxidation, and
  • The replacement of 1 molecule of NADH with 1 molecule of FADH2 in fat oxidation

Let’s explore each of these differences more closely.

Carbon Dioxide, Simply A Waste Product?

CO2 is often considered a waste product of mitochondrial respiration, but this couldn’t be farther from the truth. In fact, CO2 is one of the most protective compounds in our bodies.

The oxidation of carbohydrates produces 50% more CO2 than the oxidation of fat, which is a major difference that has a dramatic effect on the efficiency of mitochondrial respiration for a couple reasons.

For one, CO2 production is vital for the proper oxygenation of our cells.

Our cells require oxygen (O2) for efficient energy production, as oxygen acts as the final electron acceptor in the electron transport chain. In order to be delivered to our cells from our lungs, oxygen is carried through our blood in our red blood cells via a protein called hemoglobin, which is able to bind with both O2 and CO2.

In low CO2 environments, hemoglobin releases CO2 and binds with O2, which is called the Haldane effect. This allows our red blood cells to drop off CO2 and pick up O2 at our lungs. In high CO2 (or acidic) environments, hemoglobin releases O2 and binds with CO2, which is called the Bohr effect. This allows our red blood cells to offload O2 at our tissues, where it’s needed to produce energy.

So, when our cells produce more CO2, as they do from glucose oxidation, our tissues receive more O2 (1). When our cells don’t produce enough CO2, preventing enough oxygen from entering the cell, glucose is converted to lactate as opposed to ACoA and the function of the electron transport chain is impaired, drastically inhibiting energy production and increasing reactive oxygen species production (2, 3, 4, 5).

(Note: CO2 is also a potent vasodilator, which further increases oxygen delivery to our tissues.)

Second, CO2 acts as a powerful protector against reactive oxygen species (ROS), reactive nitrogen species (RNS), and lipid peroxidation (6, 7, 8).

These compounds all damage our cells and inhibit energy production, making protection against these compounds extremely important.

Considering these factors, the increased CO2 production as a result of glucose oxidation results in significantly more efficient mitochondrial respiration than fat oxidation.

NADH vs. FADH2

NADH and FADH2 are both electron carriers that donate electrons at the electron transport chain (ETC), allowing for the production of ATP. NADH donates electrons at complex I of the ETC, whereas FADH2 donates electrons at complex II, and these complexes compete for the same electron acceptor, ubiquinone.

Glucose oxidation produces around 25% more NADH and half as much FADH2 as fat oxidation. Together, this leads to a ratio of FADH2 to NADH that is around 2.5 times lower than that of fat oxidation (9, 10). This difference has substantial effects that extend throughout the processes of mitochondrial respiration.

Because FADH2 donates electrons at complex II, downstream of complex I, it reduces the amount of ubiquinone available to accept electrons at complex I, leading to a buildup of electrons at complex I. This results in two major problems.

For one, this increases the electron leakage at complex I, which increases the production of ROS, specifically superoxide (9, 10, 11).

ROS are a major cause of cellular oxidative stress, and as I’ve already mentioned, damage the cell and inhibit energy production.

Second, the buildup of electrons at complex I reduces the donation of electrons by NADH, leading to a buildup of NADH and a decrease in the ratio of NAD+ to NADH (9, 10, 11, 12).

The ratio of NAD+ to NADH is a major controller of mitochondrial respiration and is also tied to aging, cancer, diabetes, neurodegeneration, and many other diseases (13, 14, 15).

A low NAD+/NADH ratio inhibits isocitrate dehydrogenase (IDH), the rate-limiting step of the TCA cycle (aka Krebs or citric acid cycle). This slows down the activity of the TCA cycle and leads to a buildup of citrate, which inhibits phosphofructokinase (PFK), the rate-limiting step of glycolysis, while also causing a buildup of ACoA (11).

The low NAD+/NADH ratio also inhibits pyruvate dehydrogenase (PDH), the rate-limiting-step that connects glycolysis to the TCA cycle, and the buildup of ACoA further inhibits PDH (11). This directs pyruvate towards lactate rather than ACoA.

The inhibition of glucose oxidation by fat oxidation through these mechanisms is a feature of the Randle cycle and is responsible for the insulin resistance seen in response to high-fat meals and diets (16). This is, of course, an adaptive response to using fat for fuel and is not a problem per se.

However, in this state, glycolysis is inhibited to a lesser degree than PDH, resulting in an increased production of lactate which can cause problems of its own (11, 17, 18). And, the decrease in the NAD+/NADH ratio still reduces the activity of the TCA cycle through the inhibition of IDH, which slows energy production.

Overall, fat oxidation drastically reduces the efficiency of energy production, causing much less energy to be produced while increasing ROS production, which has a damaging and destabilizing effect (11, 19).

What Does This Mean For Our Health?

Fat is our backup fuel, reserved for times when carbohydrates aren’t available, such as in a state of famine or starvation. This is evidenced by the fact that the presence of carbs, or lack thereof, is what determines the relative amount of fat oxidation (20). So, when relying on fat for energy production, it’s no wonder why there are mechanisms in place to slow our energy production – it allows us to survive longer during these sorts of stressful times.

However, it’s clear that for our brain, our most energy-intensive organ, fats simply cannot efficiently provide enough energy for proper function, which is why sugars or ketones are required as fuel. Many of our other tissues, however, can still function using solely fat as fuel.

But is this ideal for health?

As I postulated in this article, energy lies at the foundation of our health and allows our bodies to properly function. And, energy deficiencies underlie virtually all the chronic health conditions we’re seeing in epidemic proportions, as well as fat gain.

Although, it’s worth pointing out that fat oxidation isn’t the most common cause of energy deficiencies.

Energy deficiencies are most commonly a result of the various factors that impair the oxidation of glucose, like PUFA or endotoxin, even in the context of adequate glucose availability. In this context, fatty acid oxidation is also partially inhibited due to the presence of high amounts of glucose and insulin.

This results in the inhibition of both glucose and fat oxidation, leading to severe energy deficiencies and extreme stress.

This is why it’s common for health to improve when switching to a low-carb or ketogenic diet, at least at first. By reducing the amount of glucose available, insulin is suppressed and fatty acid oxidation and ketone production can increase to supply enough energy to improve function.

While this is a much better situation than when both glucose and fat oxidation are inhibited, it’s still not ideal. Considering that carbohydrate oxidation provides more energy more efficiently, and energy is the driving force behind our health, providing as much energy as we can from carbohydrate oxidation is probably ideal.

But, this doesn’t mean we need to avoid fat altogether. Fat serves many purposes in our body beyond its use as a fuel source, such as its function as a structural component of our cells and its antimicrobial effects. While we can produce fat endogenously to fill these roles without consuming it, this doesn’t mean that we need to eliminate fat from our diet as long as carbohydrates are our primary fuel source.

References

Carbs vs. Fats: Which is the Better Fuel?

It’s time for the age-old debate: carbs vs. fats.

There’s a ton of disagreement on this topic with poorly supported arguments on both sides.

Most of the current recommendations are now favoring the low-carb “fat-burning approach.” This is “supported” by all sorts of nonsense, such as that “carbohydrates aren’t essential to our diets,” “carbohydrates cause blood sugar dysregulation,” “burning fat leads to fat loss,” and “our ancestors didn’t eat carbohydrates,” among others.

While I’m tempted to go through each of these ridiculous arguments right now and explain why they aren’t at all valid, I’ll have to save that for another time.

There are many differences between the effects of consuming carbohydrates and fats that can be explored, including their interactions with various hormones, effects on blood sugar, distribution throughout the body, and many other differences, as well as the variations between the different types of carbohydrates and fats. However, while these are important topics, the answer to this debate becomes quite clear when you consider it from a bioenergetic point of view.

So in this article, I’m going to focus solely on the usage of carbs and fats as fuel to produce energy. There’s quite a bit of misinformation out there about “fat-burning” versus “sugar-burning” and their effects on energy production and mitochondrial function, and I’m going to clear that up.

In order to do that, I’m going to dive into the biochemistry of carbohydrate and fat oxidation. If you want a general overview of this topic without all the biochemistry, check out this article.

Also, I’d like to preface this article by pointing out that we’re never burning only carbs or only fats, there’s always some combination of these fuels being used, but which fuel we predominantly use does make a difference.

Carbohydrate Oxidation vs. Fat Oxidation

When considering the oxidation of carbohydrates and fats through mitochondrial respiration, a majority of the process is the same – once each of these substrates is converted to acetyl-CoA (ACoA), the rest is identical.

But, there are several important differences between carbohydrate and fat oxidation that occur before they become ACoA. While these differences may seem small, they’re responsible for the significantly increased efficiency of glucose oxidation over fat oxidation.

The oxidation of carbohydrates begins with glycolysis, where glucose is eventually converted into pyruvate and then either lactate or ACoA. For each molecule of ACoA that’s produced through this process, 1 net molecule of ATP, 2 molecules of NADH, and 1 molecule of carbon dioxide (CO2) are produced.

The oxidation of fats, on the other hand, begins with beta-oxidation, where the fatty acid is converted to ACoA. For each molecule of ACoA that’s produced through this process, on average, 1 molecule of NADH and 1 molecule of FADH2 are produced.

There are two key differences here that have significant effects on mitochondrial respiration:

  • The additional CO2 production in glucose oxidation, and
  • The replacement of 1 molecule of NADH with 1 molecule of FADH2 in fat oxidation

Let’s explore each of these differences more closely.

Carbon Dioxide, Simply A Waste Product?

CO2 is often considered a waste product of mitochondrial respiration, but this couldn’t be farther from the truth. In fact, CO2 is one of the most protective compounds in our bodies.

The oxidation of carbohydrates produces 50% more CO2 than the oxidation of fat, which is a major difference that has a dramatic effect on the efficiency of mitochondrial respiration for a couple reasons.

For one, CO2 production is vital for the proper oxygenation of our cells.

Our cells require oxygen (O2) for efficient energy production, as oxygen acts as the final electron acceptor in the electron transport chain. In order to be delivered to our cells from our lungs, oxygen is carried through our blood in our red blood cells via a protein called hemoglobin, which is able to bind with both O2 and CO2.

In low CO2 environments, hemoglobin releases CO2 and binds with O2, which is called the Haldane effect. This allows our red blood cells to drop off CO2 and pick up O2 at our lungs. In high CO2 (or acidic) environments, hemoglobin releases O2 and binds with CO2, which is called the Bohr effect. This allows our red blood cells to offload O2 at our tissues, where it’s needed to produce energy.

So, when our cells produce more CO2, as they do from glucose oxidation, our tissues receive more O2 (1). When our cells don’t produce enough CO2, preventing enough oxygen from entering the cell, glucose is converted to lactate as opposed to ACoA and the function of the electron transport chain is impaired, drastically inhibiting energy production and increasing reactive oxygen species production (2, 3, 4, 5).

(Note: CO2 is also a potent vasodilator, which further increases oxygen delivery to our tissues.)

Second, CO2 acts as a powerful protector against reactive oxygen species (ROS), reactive nitrogen species (RNS), and lipid peroxidation (6, 7, 8).

These compounds all damage our cells and inhibit energy production, making protection against these compounds extremely important.

Considering these factors, the increased CO2 production as a result of glucose oxidation results in significantly more efficient mitochondrial respiration than fat oxidation.

NADH vs. FADH2

NADH and FADH2 are both electron carriers that donate electrons at the electron transport chain (ETC), allowing for the production of ATP. NADH donates electrons at complex I of the ETC, whereas FADH2 donates electrons at complex II, and these complexes compete for the same electron acceptor, ubiquinone.

Glucose oxidation produces around 25% more NADH and half as much FADH2 as fat oxidation. Together, this leads to a ratio of FADH2 to NADH that is around 2.5 times lower than that of fat oxidation (9, 10). This difference has substantial effects that extend throughout the processes of mitochondrial respiration.

Because FADH2 donates electrons at complex II, downstream of complex I, it reduces the amount of ubiquinone available to accept electrons at complex I, leading to a buildup of electrons at complex I. This results in two major problems.

For one, this increases the electron leakage at complex I, which increases the production of ROS, specifically superoxide (9, 10, 11).

ROS are a major cause of cellular oxidative stress, and as I’ve already mentioned, damage the cell and inhibit energy production.

Second, the buildup of electrons at complex I reduces the donation of electrons by NADH, leading to a buildup of NADH and a decrease in the ratio of NAD+ to NADH (9, 10, 11, 12).

The ratio of NAD+ to NADH is a major controller of mitochondrial respiration and is also tied to aging, cancer, diabetes, neurodegeneration, and many other diseases (13, 14, 15).

A low NAD+/NADH ratio inhibits isocitrate dehydrogenase (IDH), the rate-limiting step of the TCA cycle (aka Krebs or citric acid cycle). This slows down the activity of the TCA cycle and leads to a buildup of citrate, which inhibits phosphofructokinase (PFK), the rate-limiting step of glycolysis, while also causing a buildup of ACoA (11).

The low NAD+/NADH ratio also inhibits pyruvate dehydrogenase (PDH), the rate-limiting-step that connects glycolysis to the TCA cycle, and the buildup of ACoA further inhibits PDH (11). This directs pyruvate towards lactate rather than ACoA.

The inhibition of glucose oxidation by fat oxidation through these mechanisms is a feature of the Randle cycle and is responsible for the insulin resistance seen in response to high-fat meals and diets (16). This is, of course, an adaptive response to using fat for fuel and is not a problem per se.

However, in this state, glycolysis is inhibited to a lesser degree than PDH, resulting in an increased production of lactate which can cause problems of its own (11, 17, 18). And, the decrease in the NAD+/NADH ratio still reduces the activity of the TCA cycle through the inhibition of IDH, which slows energy production.

Overall, fat oxidation drastically reduces the efficiency of energy production, causing much less energy to be produced while increasing ROS production, which has a damaging and destabilizing effect (11, 19).

What Does This Mean For Our Health?

Fat is our backup fuel, reserved for times when carbohydrates aren’t available, such as in a state of famine or starvation. This is evidenced by the fact that the presence of carbs, or lack thereof, is what determines the relative amount of fat oxidation (20). So, when relying on fat for energy production, it’s no wonder why there are mechanisms in place to slow our energy production – it allows us to survive longer during these sorts of stressful times.

However, it’s clear that for our brain, our most energy-intensive organ, fats simply cannot efficiently provide enough energy for proper function, which is why sugars or ketones are required as fuel. Many of our other tissues, however, can still function using solely fat as fuel.

But is this ideal for health?

As I postulated in this article, energy lies at the foundation of our health and allows our bodies to properly function. And, energy deficiencies underlie virtually all the chronic health conditions we’re seeing in epidemic proportions, as well as fat gain.

Although, it’s worth pointing out that fat oxidation isn’t the most common cause of energy deficiencies.

Energy deficiencies are most commonly a result of the various factors that impair the oxidation of glucose, like PUFA or endotoxin, even in the context of adequate glucose availability. In this context, fatty acid oxidation is also partially inhibited due to the presence of high amounts of glucose and insulin.

This results in the inhibition of both glucose and fat oxidation, leading to severe energy deficiencies and extreme stress.

This is why it’s common for health to improve when switching to a low-carb or ketogenic diet, at least at first. By reducing the amount of glucose available, insulin is suppressed and fatty acid oxidation and ketone production can increase to supply enough energy to improve function.

While this is a much better situation than when both glucose and fat oxidation are inhibited, it’s still not ideal. Considering that carbohydrate oxidation provides more energy more efficiently, and energy is the driving force behind our health, providing as much energy as we can from carbohydrate oxidation is probably ideal.

But, this doesn’t mean we need to avoid fat altogether. Fat serves many purposes in our body beyond its use as a fuel source, such as its function as a structural component of our cells and its antimicrobial effects. While we can produce fat endogenously to fill these roles without consuming it, this doesn’t mean that we need to eliminate fat from our diet as long as carbohydrates are our primary fuel source.

References

Carbs vs. Fats: Which is the Better Fuel?

It’s time for the age-old debate: carbs vs. fats.

There’s a ton of disagreement on this topic with poorly supported arguments on both sides.

Most of the current recommendations are now favoring the low-carb “fat-burning approach.” This is “supported” by all sorts of nonsense, such as that “carbohydrates aren’t essential to our diets,” “carbohydrates cause blood sugar dysregulation,” “burning fat leads to fat loss,” and “our ancestors didn’t eat carbohydrates,” among others.

While I’m tempted to go through each of these ridiculous arguments right now and explain why they aren’t at all valid, I’ll have to save that for another time.

There are many differences between the effects of consuming carbohydrates and fats that can be explored, including their interactions with various hormones, effects on blood sugar, distribution throughout the body, and many other differences, as well as the variations between the different types of carbohydrates and fats. However, while these are important topics, the answer to this debate becomes quite clear when you consider it from a bioenergetic point of view.

So in this article, I’m going to focus solely on the usage of carbs and fats as fuel to produce energy. There’s quite a bit of misinformation out there about “fat-burning” versus “sugar-burning” and their effects on energy production and mitochondrial function, and I’m going to clear that up.

In order to do that, I’m going to dive into the biochemistry of carbohydrate and fat oxidation. If you want a general overview of this topic without all the biochemistry, check out this article.

Also, I’d like to preface this article by pointing out that we’re never burning only carbs or only fats, there’s always some combination of these fuels being used, but which fuel we predominantly use does make a difference.

Carbohydrate Oxidation vs. Fat Oxidation

When considering the oxidation of carbohydrates and fats through mitochondrial respiration, a majority of the process is the same – once each of these substrates is converted to acetyl-CoA (ACoA), the rest is identical.

But, there are several important differences between carbohydrate and fat oxidation that occur before they become ACoA. While these differences may seem small, they’re responsible for the significantly increased efficiency of glucose oxidation over fat oxidation.

The oxidation of carbohydrates begins with glycolysis, where glucose is eventually converted into pyruvate and then either lactate or ACoA. For each molecule of ACoA that’s produced through this process, 1 net molecule of ATP, 2 molecules of NADH, and 1 molecule of carbon dioxide (CO2) are produced.

The oxidation of fats, on the other hand, begins with beta-oxidation, where the fatty acid is converted to ACoA. For each molecule of ACoA that’s produced through this process, on average, 1 molecule of NADH and 1 molecule of FADH2 are produced.

There are two key differences here that have significant effects on mitochondrial respiration:

  • The additional CO2 production in glucose oxidation, and
  • The replacement of 1 molecule of NADH with 1 molecule of FADH2 in fat oxidation

Let’s explore each of these differences more closely.

Carbon Dioxide, Simply A Waste Product?

CO2 is often considered a waste product of mitochondrial respiration, but this couldn’t be farther from the truth. In fact, CO2 is one of the most protective compounds in our bodies.

The oxidation of carbohydrates produces 50% more CO2 than the oxidation of fat, which is a major difference that has a dramatic effect on the efficiency of mitochondrial respiration for a couple reasons.

For one, CO2 production is vital for the proper oxygenation of our cells.

Our cells require oxygen (O2) for efficient energy production, as oxygen acts as the final electron acceptor in the electron transport chain. In order to be delivered to our cells from our lungs, oxygen is carried through our blood in our red blood cells via a protein called hemoglobin, which is able to bind with both O2 and CO2.

In low CO2 environments, hemoglobin releases CO2 and binds with O2, which is called the Haldane effect. This allows our red blood cells to drop off CO2 and pick up O2 at our lungs. In high CO2 (or acidic) environments, hemoglobin releases O2 and binds with CO2, which is called the Bohr effect. This allows our red blood cells to offload O2 at our tissues, where it’s needed to produce energy.

So, when our cells produce more CO2, as they do from glucose oxidation, our tissues receive more O2 (1). When our cells don’t produce enough CO2, preventing enough oxygen from entering the cell, glucose is converted to lactate as opposed to ACoA and the function of the electron transport chain is impaired, drastically inhibiting energy production and increasing reactive oxygen species production (2, 3, 4, 5).

(Note: CO2 is also a potent vasodilator, which further increases oxygen delivery to our tissues.)

Second, CO2 acts as a powerful protector against reactive oxygen species (ROS), reactive nitrogen species (RNS), and lipid peroxidation (6, 7, 8).

These compounds all damage our cells and inhibit energy production, making protection against these compounds extremely important.

Considering these factors, the increased CO2 production as a result of glucose oxidation results in significantly more efficient mitochondrial respiration than fat oxidation.

NADH vs. FADH2

NADH and FADH2 are both electron carriers that donate electrons at the electron transport chain (ETC), allowing for the production of ATP. NADH donates electrons at complex I of the ETC, whereas FADH2 donates electrons at complex II, and these complexes compete for the same electron acceptor, ubiquinone.

Glucose oxidation produces around 25% more NADH and half as much FADH2 as fat oxidation. Together, this leads to a ratio of FADH2 to NADH that is around 2.5 times lower than that of fat oxidation (9, 10). This difference has substantial effects that extend throughout the processes of mitochondrial respiration.

Because FADH2 donates electrons at complex II, downstream of complex I, it reduces the amount of ubiquinone available to accept electrons at complex I, leading to a buildup of electrons at complex I. This results in two major problems.

For one, this increases the electron leakage at complex I, which increases the production of ROS, specifically superoxide (9, 10, 11).

ROS are a major cause of cellular oxidative stress, and as I’ve already mentioned, damage the cell and inhibit energy production.

Second, the buildup of electrons at complex I reduces the donation of electrons by NADH, leading to a buildup of NADH and a decrease in the ratio of NAD+ to NADH (9, 10, 11, 12).

The ratio of NAD+ to NADH is a major controller of mitochondrial respiration and is also tied to aging, cancer, diabetes, neurodegeneration, and many other diseases (13, 14, 15).

A low NAD+/NADH ratio inhibits isocitrate dehydrogenase (IDH), the rate-limiting step of the TCA cycle (aka Krebs or citric acid cycle). This slows down the activity of the TCA cycle and leads to a buildup of citrate, which inhibits phosphofructokinase (PFK), the rate-limiting step of glycolysis, while also causing a buildup of ACoA (11).

The low NAD+/NADH ratio also inhibits pyruvate dehydrogenase (PDH), the rate-limiting-step that connects glycolysis to the TCA cycle, and the buildup of ACoA further inhibits PDH (11). This directs pyruvate towards lactate rather than ACoA.

The inhibition of glucose oxidation by fat oxidation through these mechanisms is a feature of the Randle cycle and is responsible for the insulin resistance seen in response to high-fat meals and diets (16). This is, of course, an adaptive response to using fat for fuel and is not a problem per se.

However, in this state, glycolysis is inhibited to a lesser degree than PDH, resulting in an increased production of lactate which can cause problems of its own (11, 17, 18). And, the decrease in the NAD+/NADH ratio still reduces the activity of the TCA cycle through the inhibition of IDH, which slows energy production.

Overall, fat oxidation drastically reduces the efficiency of energy production, causing much less energy to be produced while increasing ROS production, which has a damaging and destabilizing effect (11, 19).

What Does This Mean For Our Health?

Fat is our backup fuel, reserved for times when carbohydrates aren’t available, such as in a state of famine or starvation. This is evidenced by the fact that the presence of carbs, or lack thereof, is what determines the relative amount of fat oxidation (20). So, when relying on fat for energy production, it’s no wonder why there are mechanisms in place to slow our energy production – it allows us to survive longer during these sorts of stressful times.

However, it’s clear that for our brain, our most energy-intensive organ, fats simply cannot efficiently provide enough energy for proper function, which is why sugars or ketones are required as fuel. Many of our other tissues, however, can still function using solely fat as fuel.

But is this ideal for health?

As I postulated in this article, energy lies at the foundation of our health and allows our bodies to properly function. And, energy deficiencies underlie virtually all the chronic health conditions we’re seeing in epidemic proportions, as well as fat gain.

Although, it’s worth pointing out that fat oxidation isn’t the most common cause of energy deficiencies.

Energy deficiencies are most commonly a result of the various factors that impair the oxidation of glucose, like PUFA or endotoxin, even in the context of adequate glucose availability. In this context, fatty acid oxidation is also partially inhibited due to the presence of high amounts of glucose and insulin.

This results in the inhibition of both glucose and fat oxidation, leading to severe energy deficiencies and extreme stress.

This is why it’s common for health to improve when switching to a low-carb or ketogenic diet, at least at first. By reducing the amount of glucose available, insulin is suppressed and fatty acid oxidation and ketone production can increase to supply enough energy to improve function.

While this is a much better situation than when both glucose and fat oxidation are inhibited, it’s still not ideal. Considering that carbohydrate oxidation provides more energy more efficiently, and energy is the driving force behind our health, providing as much energy as we can from carbohydrate oxidation is probably ideal.

But, this doesn’t mean we need to avoid fat altogether. Fat serves many purposes in our body beyond its use as a fuel source, such as its function as a structural component of our cells and its antimicrobial effects. While we can produce fat endogenously to fill these roles without consuming it, this doesn’t mean that we need to eliminate fat from our diet as long as carbohydrates are our primary fuel source.

References

Carbs vs. Fats: Which is the Better Fuel?

It’s time for the age-old debate: carbs vs. fats.

There’s a ton of disagreement on this topic with poorly supported arguments on both sides.

Most of the current recommendations are now favoring the low-carb “fat-burning approach.” This is “supported” by all sorts of nonsense, such as that “carbohydrates aren’t essential to our diets,” “carbohydrates cause blood sugar dysregulation,” “burning fat leads to fat loss,” and “our ancestors didn’t eat carbohydrates,” among others.

While I’m tempted to go through each of these ridiculous arguments right now and explain why they aren’t at all valid, I’ll have to save that for another time.

There are many differences between the effects of consuming carbohydrates and fats that can be explored, including their interactions with various hormones, effects on blood sugar, distribution throughout the body, and many other differences, as well as the variations between the different types of carbohydrates and fats. However, while these are important topics, the answer to this debate becomes quite clear when you consider it from a bioenergetic point of view.

So in this article, I’m going to focus solely on the usage of carbs and fats as fuel to produce energy. There’s quite a bit of misinformation out there about “fat-burning” versus “sugar-burning” and their effects on energy production and mitochondrial function, and I’m going to clear that up.

In order to do that, I’m going to dive into the biochemistry of carbohydrate and fat oxidation. If you want a general overview of this topic without all the biochemistry, check out this article.

Also, I’d like to preface this article by pointing out that we’re never burning only carbs or only fats, there’s always some combination of these fuels being used, but which fuel we predominantly use does make a difference.

Carbohydrate Oxidation vs. Fat Oxidation

When considering the oxidation of carbohydrates and fats through mitochondrial respiration, a majority of the process is the same – once each of these substrates is converted to acetyl-CoA (ACoA), the rest is identical.

But, there are several important differences between carbohydrate and fat oxidation that occur before they become ACoA. While these differences may seem small, they’re responsible for the significantly increased efficiency of glucose oxidation over fat oxidation.

The oxidation of carbohydrates begins with glycolysis, where glucose is eventually converted into pyruvate and then either lactate or ACoA. For each molecule of ACoA that’s produced through this process, 1 net molecule of ATP, 2 molecules of NADH, and 1 molecule of carbon dioxide (CO2) are produced.

The oxidation of fats, on the other hand, begins with beta-oxidation, where the fatty acid is converted to ACoA. For each molecule of ACoA that’s produced through this process, on average, 1 molecule of NADH and 1 molecule of FADH2 are produced.

There are two key differences here that have significant effects on mitochondrial respiration:

  • The additional CO2 production in glucose oxidation, and
  • The replacement of 1 molecule of NADH with 1 molecule of FADH2 in fat oxidation

Let’s explore each of these differences more closely.

Carbon Dioxide, Simply A Waste Product?

CO2 is often considered a waste product of mitochondrial respiration, but this couldn’t be farther from the truth. In fact, CO2 is one of the most protective compounds in our bodies.

The oxidation of carbohydrates produces 50% more CO2 than the oxidation of fat, which is a major difference that has a dramatic effect on the efficiency of mitochondrial respiration for a couple reasons.

For one, CO2 production is vital for the proper oxygenation of our cells.

Our cells require oxygen (O2) for efficient energy production, as oxygen acts as the final electron acceptor in the electron transport chain. In order to be delivered to our cells from our lungs, oxygen is carried through our blood in our red blood cells via a protein called hemoglobin, which is able to bind with both O2 and CO2.

In low CO2 environments, hemoglobin releases CO2 and binds with O2, which is called the Haldane effect. This allows our red blood cells to drop off CO2 and pick up O2 at our lungs. In high CO2 (or acidic) environments, hemoglobin releases O2 and binds with CO2, which is called the Bohr effect. This allows our red blood cells to offload O2 at our tissues, where it’s needed to produce energy.

So, when our cells produce more CO2, as they do from glucose oxidation, our tissues receive more O2 (1). When our cells don’t produce enough CO2, preventing enough oxygen from entering the cell, glucose is converted to lactate as opposed to ACoA and the function of the electron transport chain is impaired, drastically inhibiting energy production and increasing reactive oxygen species production (2, 3, 4, 5).

(Note: CO2 is also a potent vasodilator, which further increases oxygen delivery to our tissues.)

Second, CO2 acts as a powerful protector against reactive oxygen species (ROS), reactive nitrogen species (RNS), and lipid peroxidation (6, 7, 8).

These compounds all damage our cells and inhibit energy production, making protection against these compounds extremely important.

Considering these factors, the increased CO2 production as a result of glucose oxidation results in significantly more efficient mitochondrial respiration than fat oxidation.

NADH vs. FADH2

NADH and FADH2 are both electron carriers that donate electrons at the electron transport chain (ETC), allowing for the production of ATP. NADH donates electrons at complex I of the ETC, whereas FADH2 donates electrons at complex II, and these complexes compete for the same electron acceptor, ubiquinone.

Glucose oxidation produces around 25% more NADH and half as much FADH2 as fat oxidation. Together, this leads to a ratio of FADH2 to NADH that is around 2.5 times lower than that of fat oxidation (9, 10). This difference has substantial effects that extend throughout the processes of mitochondrial respiration.

Because FADH2 donates electrons at complex II, downstream of complex I, it reduces the amount of ubiquinone available to accept electrons at complex I, leading to a buildup of electrons at complex I. This results in two major problems.

For one, this increases the electron leakage at complex I, which increases the production of ROS, specifically superoxide (9, 10, 11).

ROS are a major cause of cellular oxidative stress, and as I’ve already mentioned, damage the cell and inhibit energy production.

Second, the buildup of electrons at complex I reduces the donation of electrons by NADH, leading to a buildup of NADH and a decrease in the ratio of NAD+ to NADH (9, 10, 11, 12).

The ratio of NAD+ to NADH is a major controller of mitochondrial respiration and is also tied to aging, cancer, diabetes, neurodegeneration, and many other diseases (13, 14, 15).

A low NAD+/NADH ratio inhibits isocitrate dehydrogenase (IDH), the rate-limiting step of the TCA cycle (aka Krebs or citric acid cycle). This slows down the activity of the TCA cycle and leads to a buildup of citrate, which inhibits phosphofructokinase (PFK), the rate-limiting step of glycolysis, while also causing a buildup of ACoA (11).

The low NAD+/NADH ratio also inhibits pyruvate dehydrogenase (PDH), the rate-limiting-step that connects glycolysis to the TCA cycle, and the buildup of ACoA further inhibits PDH (11). This directs pyruvate towards lactate rather than ACoA.

The inhibition of glucose oxidation by fat oxidation through these mechanisms is a feature of the Randle cycle and is responsible for the insulin resistance seen in response to high-fat meals and diets (16). This is, of course, an adaptive response to using fat for fuel and is not a problem per se.

However, in this state, glycolysis is inhibited to a lesser degree than PDH, resulting in an increased production of lactate which can cause problems of its own (11, 17, 18). And, the decrease in the NAD+/NADH ratio still reduces the activity of the TCA cycle through the inhibition of IDH, which slows energy production.

Overall, fat oxidation drastically reduces the efficiency of energy production, causing much less energy to be produced while increasing ROS production, which has a damaging and destabilizing effect (11, 19).

What Does This Mean For Our Health?

Fat is our backup fuel, reserved for times when carbohydrates aren’t available, such as in a state of famine or starvation. This is evidenced by the fact that the presence of carbs, or lack thereof, is what determines the relative amount of fat oxidation (20). So, when relying on fat for energy production, it’s no wonder why there are mechanisms in place to slow our energy production – it allows us to survive longer during these sorts of stressful times.

However, it’s clear that for our brain, our most energy-intensive organ, fats simply cannot efficiently provide enough energy for proper function, which is why sugars or ketones are required as fuel. Many of our other tissues, however, can still function using solely fat as fuel.

But is this ideal for health?

As I postulated in this article, energy lies at the foundation of our health and allows our bodies to properly function. And, energy deficiencies underlie virtually all the chronic health conditions we’re seeing in epidemic proportions, as well as fat gain.

Although, it’s worth pointing out that fat oxidation isn’t the most common cause of energy deficiencies.

Energy deficiencies are most commonly a result of the various factors that impair the oxidation of glucose, like PUFA or endotoxin, even in the context of adequate glucose availability. In this context, fatty acid oxidation is also partially inhibited due to the presence of high amounts of glucose and insulin.

This results in the inhibition of both glucose and fat oxidation, leading to severe energy deficiencies and extreme stress.

This is why it’s common for health to improve when switching to a low-carb or ketogenic diet, at least at first. By reducing the amount of glucose available, insulin is suppressed and fatty acid oxidation and ketone production can increase to supply enough energy to improve function.

While this is a much better situation than when both glucose and fat oxidation are inhibited, it’s still not ideal. Considering that carbohydrate oxidation provides more energy more efficiently, and energy is the driving force behind our health, providing as much energy as we can from carbohydrate oxidation is probably ideal.

But, this doesn’t mean we need to avoid fat altogether. Fat serves many purposes in our body beyond its use as a fuel source, such as its function as a structural component of our cells and its antimicrobial effects. While we can produce fat endogenously to fill these roles without consuming it, this doesn’t mean that we need to eliminate fat from our diet as long as carbohydrates are our primary fuel source.

References

Carbs vs. Fats: Which is the Better Fuel?

It’s time for the age-old debate: carbs vs. fats.

There’s a ton of disagreement on this topic with poorly supported arguments on both sides.

Most of the current recommendations are now favoring the low-carb “fat-burning approach.” This is “supported” by all sorts of nonsense, such as that “carbohydrates aren’t essential to our diets,” “carbohydrates cause blood sugar dysregulation,” “burning fat leads to fat loss,” and “our ancestors didn’t eat carbohydrates,” among others.

While I’m tempted to go through each of these ridiculous arguments right now and explain why they aren’t at all valid, I’ll have to save that for another time.

There are many differences between the effects of consuming carbohydrates and fats that can be explored, including their interactions with various hormones, effects on blood sugar, distribution throughout the body, and many other differences, as well as the variations between the different types of carbohydrates and fats. However, while these are important topics, the answer to this debate becomes quite clear when you consider it from a bioenergetic point of view.

So in this article, I’m going to focus solely on the usage of carbs and fats as fuel to produce energy. There’s quite a bit of misinformation out there about “fat-burning” versus “sugar-burning” and their effects on energy production and mitochondrial function, and I’m going to clear that up.

In order to do that, I’m going to dive into the biochemistry of carbohydrate and fat oxidation. If you want a general overview of this topic without all the biochemistry, check out this article.

Also, I’d like to preface this article by pointing out that we’re never burning only carbs or only fats, there’s always some combination of these fuels being used, but which fuel we predominantly use does make a difference.

Carbohydrate Oxidation vs. Fat Oxidation

When considering the oxidation of carbohydrates and fats through mitochondrial respiration, a majority of the process is the same – once each of these substrates is converted to acetyl-CoA (ACoA), the rest is identical.

But, there are several important differences between carbohydrate and fat oxidation that occur before they become ACoA. While these differences may seem small, they’re responsible for the significantly increased efficiency of glucose oxidation over fat oxidation.

The oxidation of carbohydrates begins with glycolysis, where glucose is eventually converted into pyruvate and then either lactate or ACoA. For each molecule of ACoA that’s produced through this process, 1 net molecule of ATP, 2 molecules of NADH, and 1 molecule of carbon dioxide (CO2) are produced.

The oxidation of fats, on the other hand, begins with beta-oxidation, where the fatty acid is converted to ACoA. For each molecule of ACoA that’s produced through this process, on average, 1 molecule of NADH and 1 molecule of FADH2 are produced.

There are two key differences here that have significant effects on mitochondrial respiration:

  • The additional CO2 production in glucose oxidation, and
  • The replacement of 1 molecule of NADH with 1 molecule of FADH2 in fat oxidation

Let’s explore each of these differences more closely.

Carbon Dioxide, Simply A Waste Product?

CO2 is often considered a waste product of mitochondrial respiration, but this couldn’t be farther from the truth. In fact, CO2 is one of the most protective compounds in our bodies.

The oxidation of carbohydrates produces 50% more CO2 than the oxidation of fat, which is a major difference that has a dramatic effect on the efficiency of mitochondrial respiration for a couple reasons.

For one, CO2 production is vital for the proper oxygenation of our cells.

Our cells require oxygen (O2) for efficient energy production, as oxygen acts as the final electron acceptor in the electron transport chain. In order to be delivered to our cells from our lungs, oxygen is carried through our blood in our red blood cells via a protein called hemoglobin, which is able to bind with both O2 and CO2.

In low CO2 environments, hemoglobin releases CO2 and binds with O2, which is called the Haldane effect. This allows our red blood cells to drop off CO2 and pick up O2 at our lungs. In high CO2 (or acidic) environments, hemoglobin releases O2 and binds with CO2, which is called the Bohr effect. This allows our red blood cells to offload O2 at our tissues, where it’s needed to produce energy.

So, when our cells produce more CO2, as they do from glucose oxidation, our tissues receive more O2 (1). When our cells don’t produce enough CO2, preventing enough oxygen from entering the cell, glucose is converted to lactate as opposed to ACoA and the function of the electron transport chain is impaired, drastically inhibiting energy production and increasing reactive oxygen species production (2, 3, 4, 5).

(Note: CO2 is also a potent vasodilator, which further increases oxygen delivery to our tissues.)

Second, CO2 acts as a powerful protector against reactive oxygen species (ROS), reactive nitrogen species (RNS), and lipid peroxidation (6, 7, 8).

These compounds all damage our cells and inhibit energy production, making protection against these compounds extremely important.

Considering these factors, the increased CO2 production as a result of glucose oxidation results in significantly more efficient mitochondrial respiration than fat oxidation.

NADH vs. FADH2

NADH and FADH2 are both electron carriers that donate electrons at the electron transport chain (ETC), allowing for the production of ATP. NADH donates electrons at complex I of the ETC, whereas FADH2 donates electrons at complex II, and these complexes compete for the same electron acceptor, ubiquinone.

Glucose oxidation produces around 25% more NADH and half as much FADH2 as fat oxidation. Together, this leads to a ratio of FADH2 to NADH that is around 2.5 times lower than that of fat oxidation (9, 10). This difference has substantial effects that extend throughout the processes of mitochondrial respiration.

Because FADH2 donates electrons at complex II, downstream of complex I, it reduces the amount of ubiquinone available to accept electrons at complex I, leading to a buildup of electrons at complex I. This results in two major problems.

For one, this increases the electron leakage at complex I, which increases the production of ROS, specifically superoxide (9, 10, 11).

ROS are a major cause of cellular oxidative stress, and as I’ve already mentioned, damage the cell and inhibit energy production.

Second, the buildup of electrons at complex I reduces the donation of electrons by NADH, leading to a buildup of NADH and a decrease in the ratio of NAD+ to NADH (9, 10, 11, 12).

The ratio of NAD+ to NADH is a major controller of mitochondrial respiration and is also tied to aging, cancer, diabetes, neurodegeneration, and many other diseases (13, 14, 15).

A low NAD+/NADH ratio inhibits isocitrate dehydrogenase (IDH), the rate-limiting step of the TCA cycle (aka Krebs or citric acid cycle). This slows down the activity of the TCA cycle and leads to a buildup of citrate, which inhibits phosphofructokinase (PFK), the rate-limiting step of glycolysis, while also causing a buildup of ACoA (11).

The low NAD+/NADH ratio also inhibits pyruvate dehydrogenase (PDH), the rate-limiting-step that connects glycolysis to the TCA cycle, and the buildup of ACoA further inhibits PDH (11). This directs pyruvate towards lactate rather than ACoA.

The inhibition of glucose oxidation by fat oxidation through these mechanisms is a feature of the Randle cycle and is responsible for the insulin resistance seen in response to high-fat meals and diets (16). This is, of course, an adaptive response to using fat for fuel and is not a problem per se.

However, in this state, glycolysis is inhibited to a lesser degree than PDH, resulting in an increased production of lactate which can cause problems of its own (11, 17, 18). And, the decrease in the NAD+/NADH ratio still reduces the activity of the TCA cycle through the inhibition of IDH, which slows energy production.

Overall, fat oxidation drastically reduces the efficiency of energy production, causing much less energy to be produced while increasing ROS production, which has a damaging and destabilizing effect (11, 19).

What Does This Mean For Our Health?

Fat is our backup fuel, reserved for times when carbohydrates aren’t available, such as in a state of famine or starvation. This is evidenced by the fact that the presence of carbs, or lack thereof, is what determines the relative amount of fat oxidation (20). So, when relying on fat for energy production, it’s no wonder why there are mechanisms in place to slow our energy production – it allows us to survive longer during these sorts of stressful times.

However, it’s clear that for our brain, our most energy-intensive organ, fats simply cannot efficiently provide enough energy for proper function, which is why sugars or ketones are required as fuel. Many of our other tissues, however, can still function using solely fat as fuel.

But is this ideal for health?

As I postulated in this article, energy lies at the foundation of our health and allows our bodies to properly function. And, energy deficiencies underlie virtually all the chronic health conditions we’re seeing in epidemic proportions, as well as fat gain.

Although, it’s worth pointing out that fat oxidation isn’t the most common cause of energy deficiencies.

Energy deficiencies are most commonly a result of the various factors that impair the oxidation of glucose, like PUFA or endotoxin, even in the context of adequate glucose availability. In this context, fatty acid oxidation is also partially inhibited due to the presence of high amounts of glucose and insulin.

This results in the inhibition of both glucose and fat oxidation, leading to severe energy deficiencies and extreme stress.

This is why it’s common for health to improve when switching to a low-carb or ketogenic diet, at least at first. By reducing the amount of glucose available, insulin is suppressed and fatty acid oxidation and ketone production can increase to supply enough energy to improve function.

While this is a much better situation than when both glucose and fat oxidation are inhibited, it’s still not ideal. Considering that carbohydrate oxidation provides more energy more efficiently, and energy is the driving force behind our health, providing as much energy as we can from carbohydrate oxidation is probably ideal.

But, this doesn’t mean we need to avoid fat altogether. Fat serves many purposes in our body beyond its use as a fuel source, such as its function as a structural component of our cells and its antimicrobial effects. While we can produce fat endogenously to fill these roles without consuming it, this doesn’t mean that we need to eliminate fat from our diet as long as carbohydrates are our primary fuel source.

References

Carbs vs. Fats: Which is the Better Fuel?

It’s time for the age-old debate: carbs vs. fats.

There’s a ton of disagreement on this topic with poorly supported arguments on both sides.

Most of the current recommendations are now favoring the low-carb “fat-burning approach.” This is “supported” by all sorts of nonsense, such as that “carbohydrates aren’t essential to our diets,” “carbohydrates cause blood sugar dysregulation,” “burning fat leads to fat loss,” and “our ancestors didn’t eat carbohydrates,” among others.

While I’m tempted to go through each of these ridiculous arguments right now and explain why they aren’t at all valid, I’ll have to save that for another time.

There are many differences between the effects of consuming carbohydrates and fats that can be explored, including their interactions with various hormones, effects on blood sugar, distribution throughout the body, and many other differences, as well as the variations between the different types of carbohydrates and fats. However, while these are important topics, the answer to this debate becomes quite clear when you consider it from a bioenergetic point of view.

So in this article, I’m going to focus solely on the usage of carbs and fats as fuel to produce energy. There’s quite a bit of misinformation out there about “fat-burning” versus “sugar-burning” and their effects on energy production and mitochondrial function, and I’m going to clear that up.

In order to do that, I’m going to dive into the biochemistry of carbohydrate and fat oxidation. If you want a general overview of this topic without all the biochemistry, check out this article.

Also, I’d like to preface this article by pointing out that we’re never burning only carbs or only fats, there’s always some combination of these fuels being used, but which fuel we predominantly use does make a difference.

Carbohydrate Oxidation vs. Fat Oxidation

When considering the oxidation of carbohydrates and fats through mitochondrial respiration, a majority of the process is the same – once each of these substrates is converted to acetyl-CoA (ACoA), the rest is identical.

But, there are several important differences between carbohydrate and fat oxidation that occur before they become ACoA. While these differences may seem small, they’re responsible for the significantly increased efficiency of glucose oxidation over fat oxidation.

The oxidation of carbohydrates begins with glycolysis, where glucose is eventually converted into pyruvate and then either lactate or ACoA. For each molecule of ACoA that’s produced through this process, 1 net molecule of ATP, 2 molecules of NADH, and 1 molecule of carbon dioxide (CO2) are produced.

The oxidation of fats, on the other hand, begins with beta-oxidation, where the fatty acid is converted to ACoA. For each molecule of ACoA that’s produced through this process, on average, 1 molecule of NADH and 1 molecule of FADH2 are produced.

There are two key differences here that have significant effects on mitochondrial respiration:

  • The additional CO2 production in glucose oxidation, and
  • The replacement of 1 molecule of NADH with 1 molecule of FADH2 in fat oxidation

Let’s explore each of these differences more closely.

Carbon Dioxide, Simply A Waste Product?

CO2 is often considered a waste product of mitochondrial respiration, but this couldn’t be farther from the truth. In fact, CO2 is one of the most protective compounds in our bodies.

The oxidation of carbohydrates produces 50% more CO2 than the oxidation of fat, which is a major difference that has a dramatic effect on the efficiency of mitochondrial respiration for a couple reasons.

For one, CO2 production is vital for the proper oxygenation of our cells.

Our cells require oxygen (O2) for efficient energy production, as oxygen acts as the final electron acceptor in the electron transport chain. In order to be delivered to our cells from our lungs, oxygen is carried through our blood in our red blood cells via a protein called hemoglobin, which is able to bind with both O2 and CO2.

In low CO2 environments, hemoglobin releases CO2 and binds with O2, which is called the Haldane effect. This allows our red blood cells to drop off CO2 and pick up O2 at our lungs. In high CO2 (or acidic) environments, hemoglobin releases O2 and binds with CO2, which is called the Bohr effect. This allows our red blood cells to offload O2 at our tissues, where it’s needed to produce energy.

So, when our cells produce more CO2, as they do from glucose oxidation, our tissues receive more O2 (1). When our cells don’t produce enough CO2, preventing enough oxygen from entering the cell, glucose is converted to lactate as opposed to ACoA and the function of the electron transport chain is impaired, drastically inhibiting energy production and increasing reactive oxygen species production (2, 3, 4, 5).

(Note: CO2 is also a potent vasodilator, which further increases oxygen delivery to our tissues.)

Second, CO2 acts as a powerful protector against reactive oxygen species (ROS), reactive nitrogen species (RNS), and lipid peroxidation (6, 7, 8).

These compounds all damage our cells and inhibit energy production, making protection against these compounds extremely important.

Considering these factors, the increased CO2 production as a result of glucose oxidation results in significantly more efficient mitochondrial respiration than fat oxidation.

NADH vs. FADH2

NADH and FADH2 are both electron carriers that donate electrons at the electron transport chain (ETC), allowing for the production of ATP. NADH donates electrons at complex I of the ETC, whereas FADH2 donates electrons at complex II, and these complexes compete for the same electron acceptor, ubiquinone.

Glucose oxidation produces around 25% more NADH and half as much FADH2 as fat oxidation. Together, this leads to a ratio of FADH2 to NADH that is around 2.5 times lower than that of fat oxidation (9, 10). This difference has substantial effects that extend throughout the processes of mitochondrial respiration.

Because FADH2 donates electrons at complex II, downstream of complex I, it reduces the amount of ubiquinone available to accept electrons at complex I, leading to a buildup of electrons at complex I. This results in two major problems.

For one, this increases the electron leakage at complex I, which increases the production of ROS, specifically superoxide (9, 10, 11).

ROS are a major cause of cellular oxidative stress, and as I’ve already mentioned, damage the cell and inhibit energy production.

Second, the buildup of electrons at complex I reduces the donation of electrons by NADH, leading to a buildup of NADH and a decrease in the ratio of NAD+ to NADH (9, 10, 11, 12).

The ratio of NAD+ to NADH is a major controller of mitochondrial respiration and is also tied to aging, cancer, diabetes, neurodegeneration, and many other diseases (13, 14, 15).

A low NAD+/NADH ratio inhibits isocitrate dehydrogenase (IDH), the rate-limiting step of the TCA cycle (aka Krebs or citric acid cycle). This slows down the activity of the TCA cycle and leads to a buildup of citrate, which inhibits phosphofructokinase (PFK), the rate-limiting step of glycolysis, while also causing a buildup of ACoA (11).

The low NAD+/NADH ratio also inhibits pyruvate dehydrogenase (PDH), the rate-limiting-step that connects glycolysis to the TCA cycle, and the buildup of ACoA further inhibits PDH (11). This directs pyruvate towards lactate rather than ACoA.

The inhibition of glucose oxidation by fat oxidation through these mechanisms is a feature of the Randle cycle and is responsible for the insulin resistance seen in response to high-fat meals and diets (16). This is, of course, an adaptive response to using fat for fuel and is not a problem per se.

However, in this state, glycolysis is inhibited to a lesser degree than PDH, resulting in an increased production of lactate which can cause problems of its own (11, 17, 18). And, the decrease in the NAD+/NADH ratio still reduces the activity of the TCA cycle through the inhibition of IDH, which slows energy production.

Overall, fat oxidation drastically reduces the efficiency of energy production, causing much less energy to be produced while increasing ROS production, which has a damaging and destabilizing effect (11, 19).

What Does This Mean For Our Health?

Fat is our backup fuel, reserved for times when carbohydrates aren’t available, such as in a state of famine or starvation. This is evidenced by the fact that the presence of carbs, or lack thereof, is what determines the relative amount of fat oxidation (20). So, when relying on fat for energy production, it’s no wonder why there are mechanisms in place to slow our energy production – it allows us to survive longer during these sorts of stressful times.

However, it’s clear that for our brain, our most energy-intensive organ, fats simply cannot efficiently provide enough energy for proper function, which is why sugars or ketones are required as fuel. Many of our other tissues, however, can still function using solely fat as fuel.

But is this ideal for health?

As I postulated in this article, energy lies at the foundation of our health and allows our bodies to properly function. And, energy deficiencies underlie virtually all the chronic health conditions we’re seeing in epidemic proportions, as well as fat gain.

Although, it’s worth pointing out that fat oxidation isn’t the most common cause of energy deficiencies.

Energy deficiencies are most commonly a result of the various factors that impair the oxidation of glucose, like PUFA or endotoxin, even in the context of adequate glucose availability. In this context, fatty acid oxidation is also partially inhibited due to the presence of high amounts of glucose and insulin.

This results in the inhibition of both glucose and fat oxidation, leading to severe energy deficiencies and extreme stress.

This is why it’s common for health to improve when switching to a low-carb or ketogenic diet, at least at first. By reducing the amount of glucose available, insulin is suppressed and fatty acid oxidation and ketone production can increase to supply enough energy to improve function.

While this is a much better situation than when both glucose and fat oxidation are inhibited, it’s still not ideal. Considering that carbohydrate oxidation provides more energy more efficiently, and energy is the driving force behind our health, providing as much energy as we can from carbohydrate oxidation is probably ideal.

But, this doesn’t mean we need to avoid fat altogether. Fat serves many purposes in our body beyond its use as a fuel source, such as its function as a structural component of our cells and its antimicrobial effects. While we can produce fat endogenously to fill these roles without consuming it, this doesn’t mean that we need to eliminate fat from our diet as long as carbohydrates are our primary fuel source.

References

Carbs vs. Fats: Which is the Better Fuel?

It’s time for the age-old debate: carbs vs. fats.

There’s a ton of disagreement on this topic with poorly supported arguments on both sides.

Most of the current recommendations are now favoring the low-carb “fat-burning approach.” This is “supported” by all sorts of nonsense, such as that “carbohydrates aren’t essential to our diets,” “carbohydrates cause blood sugar dysregulation,” “burning fat leads to fat loss,” and “our ancestors didn’t eat carbohydrates,” among others.

While I’m tempted to go through each of these ridiculous arguments right now and explain why they aren’t at all valid, I’ll have to save that for another time.

There are many differences between the effects of consuming carbohydrates and fats that can be explored, including their interactions with various hormones, effects on blood sugar, distribution throughout the body, and many other differences, as well as the variations between the different types of carbohydrates and fats. However, while these are important topics, the answer to this debate becomes quite clear when you consider it from a bioenergetic point of view.

So in this article, I’m going to focus solely on the usage of carbs and fats as fuel to produce energy. There’s quite a bit of misinformation out there about “fat-burning” versus “sugar-burning” and their effects on energy production and mitochondrial function, and I’m going to clear that up.

In order to do that, I’m going to dive into the biochemistry of carbohydrate and fat oxidation. If you want a general overview of this topic without all the biochemistry, check out this article.

Also, I’d like to preface this article by pointing out that we’re never burning only carbs or only fats, there’s always some combination of these fuels being used, but which fuel we predominantly use does make a difference.

Carbohydrate Oxidation vs. Fat Oxidation

When considering the oxidation of carbohydrates and fats through mitochondrial respiration, a majority of the process is the same – once each of these substrates is converted to acetyl-CoA (ACoA), the rest is identical.

But, there are several important differences between carbohydrate and fat oxidation that occur before they become ACoA. While these differences may seem small, they’re responsible for the significantly increased efficiency of glucose oxidation over fat oxidation.

The oxidation of carbohydrates begins with glycolysis, where glucose is eventually converted into pyruvate and then either lactate or ACoA. For each molecule of ACoA that’s produced through this process, 1 net molecule of ATP, 2 molecules of NADH, and 1 molecule of carbon dioxide (CO2) are produced.

The oxidation of fats, on the other hand, begins with beta-oxidation, where the fatty acid is converted to ACoA. For each molecule of ACoA that’s produced through this process, on average, 1 molecule of NADH and 1 molecule of FADH2 are produced.

There are two key differences here that have significant effects on mitochondrial respiration:

  • The additional CO2 production in glucose oxidation, and
  • The replacement of 1 molecule of NADH with 1 molecule of FADH2 in fat oxidation

Let’s explore each of these differences more closely.

Carbon Dioxide, Simply A Waste Product?

CO2 is often considered a waste product of mitochondrial respiration, but this couldn’t be farther from the truth. In fact, CO2 is one of the most protective compounds in our bodies.

The oxidation of carbohydrates produces 50% more CO2 than the oxidation of fat, which is a major difference that has a dramatic effect on the efficiency of mitochondrial respiration for a couple reasons.

For one, CO2 production is vital for the proper oxygenation of our cells.

Our cells require oxygen (O2) for efficient energy production, as oxygen acts as the final electron acceptor in the electron transport chain. In order to be delivered to our cells from our lungs, oxygen is carried through our blood in our red blood cells via a protein called hemoglobin, which is able to bind with both O2 and CO2.

In low CO2 environments, hemoglobin releases CO2 and binds with O2, which is called the Haldane effect. This allows our red blood cells to drop off CO2 and pick up O2 at our lungs. In high CO2 (or acidic) environments, hemoglobin releases O2 and binds with CO2, which is called the Bohr effect. This allows our red blood cells to offload O2 at our tissues, where it’s needed to produce energy.

So, when our cells produce more CO2, as they do from glucose oxidation, our tissues receive more O2 (1). When our cells don’t produce enough CO2, preventing enough oxygen from entering the cell, glucose is converted to lactate as opposed to ACoA and the function of the electron transport chain is impaired, drastically inhibiting energy production and increasing reactive oxygen species production (2, 3, 4, 5).

(Note: CO2 is also a potent vasodilator, which further increases oxygen delivery to our tissues.)

Second, CO2 acts as a powerful protector against reactive oxygen species (ROS), reactive nitrogen species (RNS), and lipid peroxidation (6, 7, 8).

These compounds all damage our cells and inhibit energy production, making protection against these compounds extremely important.

Considering these factors, the increased CO2 production as a result of glucose oxidation results in significantly more efficient mitochondrial respiration than fat oxidation.

NADH vs. FADH2

NADH and FADH2 are both electron carriers that donate electrons at the electron transport chain (ETC), allowing for the production of ATP. NADH donates electrons at complex I of the ETC, whereas FADH2 donates electrons at complex II, and these complexes compete for the same electron acceptor, ubiquinone.

Glucose oxidation produces around 25% more NADH and half as much FADH2 as fat oxidation. Together, this leads to a ratio of FADH2 to NADH that is around 2.5 times lower than that of fat oxidation (9, 10). This difference has substantial effects that extend throughout the processes of mitochondrial respiration.

Because FADH2 donates electrons at complex II, downstream of complex I, it reduces the amount of ubiquinone available to accept electrons at complex I, leading to a buildup of electrons at complex I. This results in two major problems.

For one, this increases the electron leakage at complex I, which increases the production of ROS, specifically superoxide (9, 10, 11).

ROS are a major cause of cellular oxidative stress, and as I’ve already mentioned, damage the cell and inhibit energy production.

Second, the buildup of electrons at complex I reduces the donation of electrons by NADH, leading to a buildup of NADH and a decrease in the ratio of NAD+ to NADH (9, 10, 11, 12).

The ratio of NAD+ to NADH is a major controller of mitochondrial respiration and is also tied to aging, cancer, diabetes, neurodegeneration, and many other diseases (13, 14, 15).

A low NAD+/NADH ratio inhibits isocitrate dehydrogenase (IDH), the rate-limiting step of the TCA cycle (aka Krebs or citric acid cycle). This slows down the activity of the TCA cycle and leads to a buildup of citrate, which inhibits phosphofructokinase (PFK), the rate-limiting step of glycolysis, while also causing a buildup of ACoA (11).

The low NAD+/NADH ratio also inhibits pyruvate dehydrogenase (PDH), the rate-limiting-step that connects glycolysis to the TCA cycle, and the buildup of ACoA further inhibits PDH (11). This directs pyruvate towards lactate rather than ACoA.

The inhibition of glucose oxidation by fat oxidation through these mechanisms is a feature of the Randle cycle and is responsible for the insulin resistance seen in response to high-fat meals and diets (16). This is, of course, an adaptive response to using fat for fuel and is not a problem per se.

However, in this state, glycolysis is inhibited to a lesser degree than PDH, resulting in an increased production of lactate which can cause problems of its own (11, 17, 18). And, the decrease in the NAD+/NADH ratio still reduces the activity of the TCA cycle through the inhibition of IDH, which slows energy production.

Overall, fat oxidation drastically reduces the efficiency of energy production, causing much less energy to be produced while increasing ROS production, which has a damaging and destabilizing effect (11, 19).

What Does This Mean For Our Health?

Fat is our backup fuel, reserved for times when carbohydrates aren’t available, such as in a state of famine or starvation. This is evidenced by the fact that the presence of carbs, or lack thereof, is what determines the relative amount of fat oxidation (20). So, when relying on fat for energy production, it’s no wonder why there are mechanisms in place to slow our energy production – it allows us to survive longer during these sorts of stressful times.

However, it’s clear that for our brain, our most energy-intensive organ, fats simply cannot efficiently provide enough energy for proper function, which is why sugars or ketones are required as fuel. Many of our other tissues, however, can still function using solely fat as fuel.

But is this ideal for health?

As I postulated in this article, energy lies at the foundation of our health and allows our bodies to properly function. And, energy deficiencies underlie virtually all the chronic health conditions we’re seeing in epidemic proportions, as well as fat gain.

Although, it’s worth pointing out that fat oxidation isn’t the most common cause of energy deficiencies.

Energy deficiencies are most commonly a result of the various factors that impair the oxidation of glucose, like PUFA or endotoxin, even in the context of adequate glucose availability. In this context, fatty acid oxidation is also partially inhibited due to the presence of high amounts of glucose and insulin.

This results in the inhibition of both glucose and fat oxidation, leading to severe energy deficiencies and extreme stress.

This is why it’s common for health to improve when switching to a low-carb or ketogenic diet, at least at first. By reducing the amount of glucose available, insulin is suppressed and fatty acid oxidation and ketone production can increase to supply enough energy to improve function.

While this is a much better situation than when both glucose and fat oxidation are inhibited, it’s still not ideal. Considering that carbohydrate oxidation provides more energy more efficiently, and energy is the driving force behind our health, providing as much energy as we can from carbohydrate oxidation is probably ideal.

But, this doesn’t mean we need to avoid fat altogether. Fat serves many purposes in our body beyond its use as a fuel source, such as its function as a structural component of our cells and its antimicrobial effects. While we can produce fat endogenously to fill these roles without consuming it, this doesn’t mean that we need to eliminate fat from our diet as long as carbohydrates are our primary fuel source.

References

Carbs vs. Fats: Which is the Better Fuel?

It’s time for the age-old debate: carbs vs. fats.

There’s a ton of disagreement on this topic with poorly supported arguments on both sides.

Most of the current recommendations are now favoring the low-carb “fat-burning approach.” This is “supported” by all sorts of nonsense, such as that “carbohydrates aren’t essential to our diets,” “carbohydrates cause blood sugar dysregulation,” “burning fat leads to fat loss,” and “our ancestors didn’t eat carbohydrates,” among others.

While I’m tempted to go through each of these ridiculous arguments right now and explain why they aren’t at all valid, I’ll have to save that for another time.

There are many differences between the effects of consuming carbohydrates and fats that can be explored, including their interactions with various hormones, effects on blood sugar, distribution throughout the body, and many other differences, as well as the variations between the different types of carbohydrates and fats. However, while these are important topics, the answer to this debate becomes quite clear when you consider it from a bioenergetic point of view.

So in this article, I’m going to focus solely on the usage of carbs and fats as fuel to produce energy. There’s quite a bit of misinformation out there about “fat-burning” versus “sugar-burning” and their effects on energy production and mitochondrial function, and I’m going to clear that up.

In order to do that, I’m going to dive into the biochemistry of carbohydrate and fat oxidation. If you want a general overview of this topic without all the biochemistry, check out this article.

Also, I’d like to preface this article by pointing out that we’re never burning only carbs or only fats, there’s always some combination of these fuels being used, but which fuel we predominantly use does make a difference.

Carbohydrate Oxidation vs. Fat Oxidation

When considering the oxidation of carbohydrates and fats through mitochondrial respiration, a majority of the process is the same – once each of these substrates is converted to acetyl-CoA (ACoA), the rest is identical.

But, there are several important differences between carbohydrate and fat oxidation that occur before they become ACoA. While these differences may seem small, they’re responsible for the significantly increased efficiency of glucose oxidation over fat oxidation.

The oxidation of carbohydrates begins with glycolysis, where glucose is eventually converted into pyruvate and then either lactate or ACoA. For each molecule of ACoA that’s produced through this process, 1 net molecule of ATP, 2 molecules of NADH, and 1 molecule of carbon dioxide (CO2) are produced.

The oxidation of fats, on the other hand, begins with beta-oxidation, where the fatty acid is converted to ACoA. For each molecule of ACoA that’s produced through this process, on average, 1 molecule of NADH and 1 molecule of FADH2 are produced.

There are two key differences here that have significant effects on mitochondrial respiration:

  • The additional CO2 production in glucose oxidation, and
  • The replacement of 1 molecule of NADH with 1 molecule of FADH2 in fat oxidation

Let’s explore each of these differences more closely.

Carbon Dioxide, Simply A Waste Product?

CO2 is often considered a waste product of mitochondrial respiration, but this couldn’t be farther from the truth. In fact, CO2 is one of the most protective compounds in our bodies.

The oxidation of carbohydrates produces 50% more CO2 than the oxidation of fat, which is a major difference that has a dramatic effect on the efficiency of mitochondrial respiration for a couple reasons.

For one, CO2 production is vital for the proper oxygenation of our cells.

Our cells require oxygen (O2) for efficient energy production, as oxygen acts as the final electron acceptor in the electron transport chain. In order to be delivered to our cells from our lungs, oxygen is carried through our blood in our red blood cells via a protein called hemoglobin, which is able to bind with both O2 and CO2.

In low CO2 environments, hemoglobin releases CO2 and binds with O2, which is called the Haldane effect. This allows our red blood cells to drop off CO2 and pick up O2 at our lungs. In high CO2 (or acidic) environments, hemoglobin releases O2 and binds with CO2, which is called the Bohr effect. This allows our red blood cells to offload O2 at our tissues, where it’s needed to produce energy.

So, when our cells produce more CO2, as they do from glucose oxidation, our tissues receive more O2 (1). When our cells don’t produce enough CO2, preventing enough oxygen from entering the cell, glucose is converted to lactate as opposed to ACoA and the function of the electron transport chain is impaired, drastically inhibiting energy production and increasing reactive oxygen species production (2, 3, 4, 5).

(Note: CO2 is also a potent vasodilator, which further increases oxygen delivery to our tissues.)

Second, CO2 acts as a powerful protector against reactive oxygen species (ROS), reactive nitrogen species (RNS), and lipid peroxidation (6, 7, 8).

These compounds all damage our cells and inhibit energy production, making protection against these compounds extremely important.

Considering these factors, the increased CO2 production as a result of glucose oxidation results in significantly more efficient mitochondrial respiration than fat oxidation.

NADH vs. FADH2

NADH and FADH2 are both electron carriers that donate electrons at the electron transport chain (ETC), allowing for the production of ATP. NADH donates electrons at complex I of the ETC, whereas FADH2 donates electrons at complex II, and these complexes compete for the same electron acceptor, ubiquinone.

Glucose oxidation produces around 25% more NADH and half as much FADH2 as fat oxidation. Together, this leads to a ratio of FADH2 to NADH that is around 2.5 times lower than that of fat oxidation (9, 10). This difference has substantial effects that extend throughout the processes of mitochondrial respiration.

Because FADH2 donates electrons at complex II, downstream of complex I, it reduces the amount of ubiquinone available to accept electrons at complex I, leading to a buildup of electrons at complex I. This results in two major problems.

For one, this increases the electron leakage at complex I, which increases the production of ROS, specifically superoxide (9, 10, 11).

ROS are a major cause of cellular oxidative stress, and as I’ve already mentioned, damage the cell and inhibit energy production.

Second, the buildup of electrons at complex I reduces the donation of electrons by NADH, leading to a buildup of NADH and a decrease in the ratio of NAD+ to NADH (9, 10, 11, 12).

The ratio of NAD+ to NADH is a major controller of mitochondrial respiration and is also tied to aging, cancer, diabetes, neurodegeneration, and many other diseases (13, 14, 15).

A low NAD+/NADH ratio inhibits isocitrate dehydrogenase (IDH), the rate-limiting step of the TCA cycle (aka Krebs or citric acid cycle). This slows down the activity of the TCA cycle and leads to a buildup of citrate, which inhibits phosphofructokinase (PFK), the rate-limiting step of glycolysis, while also causing a buildup of ACoA (11).

The low NAD+/NADH ratio also inhibits pyruvate dehydrogenase (PDH), the rate-limiting-step that connects glycolysis to the TCA cycle, and the buildup of ACoA further inhibits PDH (11). This directs pyruvate towards lactate rather than ACoA.

The inhibition of glucose oxidation by fat oxidation through these mechanisms is a feature of the Randle cycle and is responsible for the insulin resistance seen in response to high-fat meals and diets (16). This is, of course, an adaptive response to using fat for fuel and is not a problem per se.

However, in this state, glycolysis is inhibited to a lesser degree than PDH, resulting in an increased production of lactate which can cause problems of its own (11, 17, 18). And, the decrease in the NAD+/NADH ratio still reduces the activity of the TCA cycle through the inhibition of IDH, which slows energy production.

Overall, fat oxidation drastically reduces the efficiency of energy production, causing much less energy to be produced while increasing ROS production, which has a damaging and destabilizing effect (11, 19).

What Does This Mean For Our Health?

Fat is our backup fuel, reserved for times when carbohydrates aren’t available, such as in a state of famine or starvation. This is evidenced by the fact that the presence of carbs, or lack thereof, is what determines the relative amount of fat oxidation (20). So, when relying on fat for energy production, it’s no wonder why there are mechanisms in place to slow our energy production – it allows us to survive longer during these sorts of stressful times.

However, it’s clear that for our brain, our most energy-intensive organ, fats simply cannot efficiently provide enough energy for proper function, which is why sugars or ketones are required as fuel. Many of our other tissues, however, can still function using solely fat as fuel.

But is this ideal for health?

As I postulated in this article, energy lies at the foundation of our health and allows our bodies to properly function. And, energy deficiencies underlie virtually all the chronic health conditions we’re seeing in epidemic proportions, as well as fat gain.

Although, it’s worth pointing out that fat oxidation isn’t the most common cause of energy deficiencies.

Energy deficiencies are most commonly a result of the various factors that impair the oxidation of glucose, like PUFA or endotoxin, even in the context of adequate glucose availability. In this context, fatty acid oxidation is also partially inhibited due to the presence of high amounts of glucose and insulin.

This results in the inhibition of both glucose and fat oxidation, leading to severe energy deficiencies and extreme stress.

This is why it’s common for health to improve when switching to a low-carb or ketogenic diet, at least at first. By reducing the amount of glucose available, insulin is suppressed and fatty acid oxidation and ketone production can increase to supply enough energy to improve function.

While this is a much better situation than when both glucose and fat oxidation are inhibited, it’s still not ideal. Considering that carbohydrate oxidation provides more energy more efficiently, and energy is the driving force behind our health, providing as much energy as we can from carbohydrate oxidation is probably ideal.

But, this doesn’t mean we need to avoid fat altogether. Fat serves many purposes in our body beyond its use as a fuel source, such as its function as a structural component of our cells and its antimicrobial effects. While we can produce fat endogenously to fill these roles without consuming it, this doesn’t mean that we need to eliminate fat from our diet as long as carbohydrates are our primary fuel source.

References

It All Comes Down To Energy

Modern biology centers around a reductionist, mechanical view of the human body that permeates both conventional and alternative medicine.

Each bodily system is considered to be separate and independent from one another. The function of the heart is unrelated to the function of the brain which is unrelated to the function of the liver, and so on.

This leads to the treatment of symptoms, which has become the primary focus of conventional medicine. If cholesterol levels are high, a cholesterol-lowering drug is prescribed. If blood pressure is high, a blood-pressure-lowering drug is prescribed. If the immune system is overactive, an immunosuppressive-drug is prescribed.

And what’s considered to cause the modern epidemic of symptoms and diseases? Typically, the answer is genetics.

(It is becoming slightly more common to consider lifestyle factors as a minor contributor to some diseases, but there’s still very little focus on these factors.)

Alternative medicines often follow a similar path, where medications are substituted with “natural” supplements or other symptom-based treatments. While there may be slightly more emphasis on lifestyle factors, many people in the alternative medicine community are taking handfuls of supplements every day, each one for a different symptom.

Many other non-conventional medicines, like integrative and functional medicine, also fall into the same reductionist tendencies. They might not be as quick to prescribe medications or supplements and they may have more emphasis on lifestyle factors, but there’s still a focus on independent causes for various conditions.

In these forms of medicine, there’s often a wild goose chase for the cause of a symptom or condition. An endless search ensues to find some form of nutrient deficiency, hormonal imbalance, mold toxin exposure, EMF exposure, gut infection, heavy metal toxicity, or other environmental harm, with the solution being to remove that causative factor. They still miss that all of the problems and their causes fall under the same umbrella… energy.

 

Why Energy?

Energy is the driving force behind all our functions and our entire structure. As such, it also serves as the unifying principle that underlies our health.

Energy allows us to breathe, think, digest food, sleep, heal injuries, move, and just about anything else you can think of. It also maintains our structure, from the structure of every individual cell to the structure of our muscles, bones, organs, fascia, skin, hair, nails, and all our other tissues.

It’s therefore logical, but perhaps counterintuitive, that virtually any condition or symptom that we experience is due to a lack of energy, which inhibits proper function and structure.

That’s right, everything from fatigue to autoimmune conditions (1, 2, 3), diabetes and insulin resistance (4, 5, 6, 7), obesity (8), cancer (9), hypertension, allergies, fibromyalgia, neuropsychiatric and neurodegenerative conditions (10, 11, 12) like Alzheimer’s, Parkinson’s, ALS, multiple sclerosis, Huntington’s, depression, bipolar disorder, schizophrenia, and autism, and pretty much every other condition can be traced back to an energy deficiency (13).

So, it makes infinitely more sense to shift our focus away from the individual symptoms, conditions, and causes, and towards a bioenergetic view of health.

 

A Bioenergetic View of Health

By focusing on how our bodies produce and use energy, we can determine how to best reverse energy deficiencies.

Energy is produced in the mitochondria, or “engines,” of our cells through a process called respiration. This process uses fuel from food, like carbohydrates and fats, along with other nutrients, like vitamins, minerals, and oxygen, to produce energy. This energy is held in a molecule called ATP.

(In future articles I’ll explore mitochondrial respiration more closely, including the differences between the oxidation of carbs and fats and other inputs that affect these processes.)

The energy produced from mitochondrial respiration is then used to perform all our functions. This includes our basic functions like breathing and keeping our heart beating, as well as maintaining our structure.

Energy is also used to handle stressors, which are any external energy demands. This includes physical activity, like exercise, and mental activity, like problem-solving and processing emotions, in addition to handling damage from things like infections, EMFs, or mold and detoxifying toxins like endotoxin.

In other words, this is why these various “causes” of different diseases aren’t independent from one another – they all exert their effects through a common means: depleting our energy supply.

When we don’t have enough energy to handle these stressors, perform our basic functions, and maintain our structure, we begin to have problems. The energy to handle these functions has to come from somewhere, and it typically comes from the maintenance and integrity of our structure. This causes deterioration over time and inhibits proper function, which eventually leads to the chronic conditions we see today in epidemic proportions.

In order to prevent this from happening and even reverse it, we have to improve mitochondrial respiration to produce more energy and reduce our stressors so that more energy is left to repair and maintain our structure.

 

The Many Dangers of Energy Deficiencies

We’ve already talked about how a lack of energy underlies the chronic conditions we’re seeing today in epidemic proportions, but energy affects all aspects of our health.

Because energy is the driving force behind all our functions and our entire structure, a lack of energy can result in all sorts of symptoms. This includes cold hands and feet or always feeling cold, fatigue, weight gain, muscle loss, hair loss, lack of libido, irritability and unstable mood, difficulty concentrating, weak hair and nails, hair loss, dry skin, insomnia, constant hunger or cravings, a lack of appetite, chronic infections, depression, PMS, headaches and migraines, swelling and edema, infertility, and many more common symptoms.

Virtually all of these symptoms were seen in the Minnesota Starvation Experiment, a study dedicated to figuring out what happens when we starve our bodies of energy (14). In this experiment, which was performed in the 1940s, participants were put on diets of around 1,800 calories per day for 6 months. This reduced-calorie diet isn’t too far off from commonly recommended fat-loss diets today, based on the participants’ height and weight.

The effects of this reduced-calorie diet were astounding, and completely changed the lives of the participants. Their health deteriorated to an incredible extent and they experienced all sorts of symptoms, including most of the ones mentioned above. It took between 2 months and 2 years of eating as much as 4,000-5,000 calories per day following the experiment for the participants to fully recover.

This experiment studied energy deficiency in the context of a low-calorie diet, which is a surefire way to reduce available energy. But, energy deficiencies are extraordinarily common nowadays even when consuming normal- or high-calorie diets.

Mitochondrial respiration, or energy production, can be inhibited by numerous factors, such as PUFA, nutrient deficiencies, and endotoxin. So even if we’re eating enough food, we still may not be converting it to usable energy. (This is what underlies fat gain, as I’ve explained in several articles.)

This is not even considering the excessive amounts of stressors that our bodies must use energy to handle, like psychological stress, environmental toxins, and EMFs.

Increasing our energy supply by improving mitochondrial respiration and reducing excessive energy demands is the key to resolving the more minor symptoms of energy deficiency, such as cold hands and feet, as well as the larger symptoms, like fat gain, infertility, and chronic conditions.

How exactly do we do that?

Well, this is the question.

And there’s not a simple answer.

This process is affected by pretty much everything in our internal and external environment, from the food we eat to the amount of sunlight we get. Of course, this can’t all be explained in one go, which is why energy is a theme that I come back to in pretty much every one of my articles.

Plus, there’s all sorts of ridiculousness out there when it comes to improving mitochondrial function, including completely misguided recommendations like ketogenic diets and fasting, which often steer people astray. I’ll cover these topics in future articles as well.

 

In the meantime, you can check out the free health and energy balance mini-course, which you can sign up for below! In this mini-course, I outline several of the more important factors affecting energy production and usage, how they affect our health, and what you can do about them.

 

References

It All Comes Down To Energy

Modern biology centers around a reductionist, mechanical view of the human body that permeates both conventional and alternative medicine.

Each bodily system is considered to be separate and independent from one another. The function of the heart is unrelated to the function of the brain which is unrelated to the function of the liver, and so on.

This leads to the treatment of symptoms, which has become the primary focus of conventional medicine. If cholesterol levels are high, a cholesterol-lowering drug is prescribed. If blood pressure is high, a blood-pressure-lowering drug is prescribed. If the immune system is overactive, an immunosuppressive-drug is prescribed.

And what’s considered to cause the modern epidemic of symptoms and diseases? Typically, the answer is genetics.

(It is becoming slightly more common to consider lifestyle factors as a minor contributor to some diseases, but there’s still very little focus on these factors.)

Alternative medicines often follow a similar path, where medications are substituted with “natural” supplements or other symptom-based treatments. While there may be slightly more emphasis on lifestyle factors, many people in the alternative medicine community are taking handfuls of supplements every day, each one for a different symptom.

Many other non-conventional medicines, like integrative and functional medicine, also fall into the same reductionist tendencies. They might not be as quick to prescribe medications or supplements and they may have more emphasis on lifestyle factors, but there’s still a focus on independent causes for various conditions.

In these forms of medicine, there’s often a wild goose chase for the cause of a symptom or condition. An endless search ensues to find some form of nutrient deficiency, hormonal imbalance, mold toxin exposure, EMF exposure, gut infection, heavy metal toxicity, or other environmental harm, with the solution being to remove that causative factor. They still miss that all of the problems and their causes fall under the same umbrella… energy.

 

Why Energy?

Energy is the driving force behind all our functions and our entire structure. As such, it also serves as the unifying principle that underlies our health.

Energy allows us to breathe, think, digest food, sleep, heal injuries, move, and just about anything else you can think of. It also maintains our structure, from the structure of every individual cell to the structure of our muscles, bones, organs, fascia, skin, hair, nails, and all our other tissues.

It’s therefore logical, but perhaps counterintuitive, that virtually any condition or symptom that we experience is due to a lack of energy, which inhibits proper function and structure.

That’s right, everything from fatigue to autoimmune conditions (1, 2, 3), diabetes and insulin resistance (4, 5, 6, 7), obesity (8), cancer (9), hypertension, allergies, fibromyalgia, neuropsychiatric and neurodegenerative conditions (10, 11, 12) like Alzheimer’s, Parkinson’s, ALS, multiple sclerosis, Huntington’s, depression, bipolar disorder, schizophrenia, and autism, and pretty much every other condition can be traced back to an energy deficiency (13).

So, it makes infinitely more sense to shift our focus away from the individual symptoms, conditions, and causes, and towards a bioenergetic view of health.

 

A Bioenergetic View of Health

By focusing on how our bodies produce and use energy, we can determine how to best reverse energy deficiencies.

Energy is produced in the mitochondria, or “engines,” of our cells through a process called respiration. This process uses fuel from food, like carbohydrates and fats, along with other nutrients, like vitamins, minerals, and oxygen, to produce energy. This energy is held in a molecule called ATP.

(In future articles I’ll explore mitochondrial respiration more closely, including the differences between the oxidation of carbs and fats and other inputs that affect these processes.)

The energy produced from mitochondrial respiration is then used to perform all our functions. This includes our basic functions like breathing and keeping our heart beating, as well as maintaining our structure.

Energy is also used to handle stressors, which are any external energy demands. This includes physical activity, like exercise, and mental activity, like problem-solving and processing emotions, in addition to handling damage from things like infections, EMFs, or mold and detoxifying toxins like endotoxin.

In other words, this is why these various “causes” of different diseases aren’t independent from one another – they all exert their effects through a common means: depleting our energy supply.

When we don’t have enough energy to handle these stressors, perform our basic functions, and maintain our structure, we begin to have problems. The energy to handle these functions has to come from somewhere, and it typically comes from the maintenance and integrity of our structure. This causes deterioration over time and inhibits proper function, which eventually leads to the chronic conditions we see today in epidemic proportions.

In order to prevent this from happening and even reverse it, we have to improve mitochondrial respiration to produce more energy and reduce our stressors so that more energy is left to repair and maintain our structure.

 

The Many Dangers of Energy Deficiencies

We’ve already talked about how a lack of energy underlies the chronic conditions we’re seeing today in epidemic proportions, but energy affects all aspects of our health.

Because energy is the driving force behind all our functions and our entire structure, a lack of energy can result in all sorts of symptoms. This includes cold hands and feet or always feeling cold, fatigue, weight gain, muscle loss, hair loss, lack of libido, irritability and unstable mood, difficulty concentrating, weak hair and nails, hair loss, dry skin, insomnia, constant hunger or cravings, a lack of appetite, chronic infections, depression, PMS, headaches and migraines, swelling and edema, infertility, and many more common symptoms.

Virtually all of these symptoms were seen in the Minnesota Starvation Experiment, a study dedicated to figuring out what happens when we starve our bodies of energy (14). In this experiment, which was performed in the 1940s, participants were put on diets of around 1,800 calories per day for 6 months. This reduced-calorie diet isn’t too far off from commonly recommended fat-loss diets today, based on the participants’ height and weight.

The effects of this reduced-calorie diet were astounding, and completely changed the lives of the participants. Their health deteriorated to an incredible extent and they experienced all sorts of symptoms, including most of the ones mentioned above. It took between 2 months and 2 years of eating as much as 4,000-5,000 calories per day following the experiment for the participants to fully recover.

This experiment studied energy deficiency in the context of a low-calorie diet, which is a surefire way to reduce available energy. But, energy deficiencies are extraordinarily common nowadays even when consuming normal- or high-calorie diets.

Mitochondrial respiration, or energy production, can be inhibited by numerous factors, such as PUFA, nutrient deficiencies, and endotoxin. So even if we’re eating enough food, we still may not be converting it to usable energy. (This is what underlies fat gain, as I’ve explained in several articles.)

This is not even considering the excessive amounts of stressors that our bodies must use energy to handle, like psychological stress, environmental toxins, and EMFs.

Increasing our energy supply by improving mitochondrial respiration and reducing excessive energy demands is the key to resolving the more minor symptoms of energy deficiency, such as cold hands and feet, as well as the larger symptoms, like fat gain, infertility, and chronic conditions.

How exactly do we do that?

Well, this is the question.

And there’s not a simple answer.

This process is affected by pretty much everything in our internal and external environment, from the food we eat to the amount of sunlight we get. Of course, this can’t all be explained in one go, which is why energy is a theme that I come back to in pretty much every one of my articles.

Plus, there’s all sorts of ridiculousness out there when it comes to improving mitochondrial function, including completely misguided recommendations like ketogenic diets and fasting, which often steer people astray. I’ll cover these topics in future articles as well.

 

In the meantime, you can check out the free health and energy balance mini-course, which you can sign up for below! In this mini-course, I outline several of the more important factors affecting energy production and usage, how they affect our health, and what you can do about them.

 

References

It All Comes Down To Energy

Modern biology centers around a reductionist, mechanical view of the human body that permeates both conventional and alternative medicine.

Each bodily system is considered to be separate and independent from one another. The function of the heart is unrelated to the function of the brain which is unrelated to the function of the liver, and so on.

This leads to the treatment of symptoms, which has become the primary focus of conventional medicine. If cholesterol levels are high, a cholesterol-lowering drug is prescribed. If blood pressure is high, a blood-pressure-lowering drug is prescribed. If the immune system is overactive, an immunosuppressive-drug is prescribed.

And what’s considered to cause the modern epidemic of symptoms and diseases? Typically, the answer is genetics.

(It is becoming slightly more common to consider lifestyle factors as a minor contributor to some diseases, but there’s still very little focus on these factors.)

Alternative medicines often follow a similar path, where medications are substituted with “natural” supplements or other symptom-based treatments. While there may be slightly more emphasis on lifestyle factors, many people in the alternative medicine community are taking handfuls of supplements every day, each one for a different symptom.

Many other non-conventional medicines, like integrative and functional medicine, also fall into the same reductionist tendencies. They might not be as quick to prescribe medications or supplements and they may have more emphasis on lifestyle factors, but there’s still a focus on independent causes for various conditions.

In these forms of medicine, there’s often a wild goose chase for the cause of a symptom or condition. An endless search ensues to find some form of nutrient deficiency, hormonal imbalance, mold toxin exposure, EMF exposure, gut infection, heavy metal toxicity, or other environmental harm, with the solution being to remove that causative factor. They still miss that all of the problems and their causes fall under the same umbrella… energy.

 

Why Energy?

Energy is the driving force behind all our functions and our entire structure. As such, it also serves as the unifying principle that underlies our health.

Energy allows us to breathe, think, digest food, sleep, heal injuries, move, and just about anything else you can think of. It also maintains our structure, from the structure of every individual cell to the structure of our muscles, bones, organs, fascia, skin, hair, nails, and all our other tissues.

It’s therefore logical, but perhaps counterintuitive, that virtually any condition or symptom that we experience is due to a lack of energy, which inhibits proper function and structure.

That’s right, everything from fatigue to autoimmune conditions (1, 2, 3), diabetes and insulin resistance (4, 5, 6, 7), obesity (8), cancer (9), hypertension, allergies, fibromyalgia, neuropsychiatric and neurodegenerative conditions (10, 11, 12) like Alzheimer’s, Parkinson’s, ALS, multiple sclerosis, Huntington’s, depression, bipolar disorder, schizophrenia, and autism, and pretty much every other condition can be traced back to an energy deficiency (13).

So, it makes infinitely more sense to shift our focus away from the individual symptoms, conditions, and causes, and towards a bioenergetic view of health.

 

A Bioenergetic View of Health

By focusing on how our bodies produce and use energy, we can determine how to best reverse energy deficiencies.

Energy is produced in the mitochondria, or “engines,” of our cells through a process called respiration. This process uses fuel from food, like carbohydrates and fats, along with other nutrients, like vitamins, minerals, and oxygen, to produce energy. This energy is held in a molecule called ATP.

(In future articles I’ll explore mitochondrial respiration more closely, including the differences between the oxidation of carbs and fats and other inputs that affect these processes.)

The energy produced from mitochondrial respiration is then used to perform all our functions. This includes our basic functions like breathing and keeping our heart beating, as well as maintaining our structure.

Energy is also used to handle stressors, which are any external energy demands. This includes physical activity, like exercise, and mental activity, like problem-solving and processing emotions, in addition to handling damage from things like infections, EMFs, or mold and detoxifying toxins like endotoxin.

In other words, this is why these various “causes” of different diseases aren’t independent from one another – they all exert their effects through a common means: depleting our energy supply.

When we don’t have enough energy to handle these stressors, perform our basic functions, and maintain our structure, we begin to have problems. The energy to handle these functions has to come from somewhere, and it typically comes from the maintenance and integrity of our structure. This causes deterioration over time and inhibits proper function, which eventually leads to the chronic conditions we see today in epidemic proportions.

In order to prevent this from happening and even reverse it, we have to improve mitochondrial respiration to produce more energy and reduce our stressors so that more energy is left to repair and maintain our structure.

 

The Many Dangers of Energy Deficiencies

We’ve already talked about how a lack of energy underlies the chronic conditions we’re seeing today in epidemic proportions, but energy affects all aspects of our health.

Because energy is the driving force behind all our functions and our entire structure, a lack of energy can result in all sorts of symptoms. This includes cold hands and feet or always feeling cold, fatigue, weight gain, muscle loss, hair loss, lack of libido, irritability and unstable mood, difficulty concentrating, weak hair and nails, hair loss, dry skin, insomnia, constant hunger or cravings, a lack of appetite, chronic infections, depression, PMS, headaches and migraines, swelling and edema, infertility, and many more common symptoms.

Virtually all of these symptoms were seen in the Minnesota Starvation Experiment, a study dedicated to figuring out what happens when we starve our bodies of energy (14). In this experiment, which was performed in the 1940s, participants were put on diets of around 1,800 calories per day for 6 months. This reduced-calorie diet isn’t too far off from commonly recommended fat-loss diets today, based on the participants’ height and weight.

The effects of this reduced-calorie diet were astounding, and completely changed the lives of the participants. Their health deteriorated to an incredible extent and they experienced all sorts of symptoms, including most of the ones mentioned above. It took between 2 months and 2 years of eating as much as 4,000-5,000 calories per day following the experiment for the participants to fully recover.

This experiment studied energy deficiency in the context of a low-calorie diet, which is a surefire way to reduce available energy. But, energy deficiencies are extraordinarily common nowadays even when consuming normal- or high-calorie diets.

Mitochondrial respiration, or energy production, can be inhibited by numerous factors, such as PUFA, nutrient deficiencies, and endotoxin. So even if we’re eating enough food, we still may not be converting it to usable energy. (This is what underlies fat gain, as I’ve explained in several articles.)

This is not even considering the excessive amounts of stressors that our bodies must use energy to handle, like psychological stress, environmental toxins, and EMFs.

Increasing our energy supply by improving mitochondrial respiration and reducing excessive energy demands is the key to resolving the more minor symptoms of energy deficiency, such as cold hands and feet, as well as the larger symptoms, like fat gain, infertility, and chronic conditions.

How exactly do we do that?

Well, this is the question.

And there’s not a simple answer.

This process is affected by pretty much everything in our internal and external environment, from the food we eat to the amount of sunlight we get. Of course, this can’t all be explained in one go, which is why energy is a theme that I come back to in pretty much every one of my articles.

Plus, there’s all sorts of ridiculousness out there when it comes to improving mitochondrial function, including completely misguided recommendations like ketogenic diets and fasting, which often steer people astray. I’ll cover these topics in future articles as well.

 

In the meantime, you can check out the free health and energy balance mini-course, which you can sign up for below! In this mini-course, I outline several of the more important factors affecting energy production and usage, how they affect our health, and what you can do about them.

 

References

It All Comes Down To Energy

Modern biology centers around a reductionist, mechanical view of the human body that permeates both conventional and alternative medicine.

Each bodily system is considered to be separate and independent from one another. The function of the heart is unrelated to the function of the brain which is unrelated to the function of the liver, and so on.

This leads to the treatment of symptoms, which has become the primary focus of conventional medicine. If cholesterol levels are high, a cholesterol-lowering drug is prescribed. If blood pressure is high, a blood-pressure-lowering drug is prescribed. If the immune system is overactive, an immunosuppressive-drug is prescribed.

And what’s considered to cause the modern epidemic of symptoms and diseases? Typically, the answer is genetics.

(It is becoming slightly more common to consider lifestyle factors as a minor contributor to some diseases, but there’s still very little focus on these factors.)

Alternative medicines often follow a similar path, where medications are substituted with “natural” supplements or other symptom-based treatments. While there may be slightly more emphasis on lifestyle factors, many people in the alternative medicine community are taking handfuls of supplements every day, each one for a different symptom.

Many other non-conventional medicines, like integrative and functional medicine, also fall into the same reductionist tendencies. They might not be as quick to prescribe medications or supplements and they may have more emphasis on lifestyle factors, but there’s still a focus on independent causes for various conditions.

In these forms of medicine, there’s often a wild goose chase for the cause of a symptom or condition. An endless search ensues to find some form of nutrient deficiency, hormonal imbalance, mold toxin exposure, EMF exposure, gut infection, heavy metal toxicity, or other environmental harm, with the solution being to remove that causative factor. They still miss that all of the problems and their causes fall under the same umbrella… energy.

 

Why Energy?

Energy is the driving force behind all our functions and our entire structure. As such, it also serves as the unifying principle that underlies our health.

Energy allows us to breathe, think, digest food, sleep, heal injuries, move, and just about anything else you can think of. It also maintains our structure, from the structure of every individual cell to the structure of our muscles, bones, organs, fascia, skin, hair, nails, and all our other tissues.

It’s therefore logical, but perhaps counterintuitive, that virtually any condition or symptom that we experience is due to a lack of energy, which inhibits proper function and structure.

That’s right, everything from fatigue to autoimmune conditions (1, 2, 3), diabetes and insulin resistance (4, 5, 6, 7), obesity (8), cancer (9), hypertension, allergies, fibromyalgia, neuropsychiatric and neurodegenerative conditions (10, 11, 12) like Alzheimer’s, Parkinson’s, ALS, multiple sclerosis, Huntington’s, depression, bipolar disorder, schizophrenia, and autism, and pretty much every other condition can be traced back to an energy deficiency (13).

So, it makes infinitely more sense to shift our focus away from the individual symptoms, conditions, and causes, and towards a bioenergetic view of health.

 

A Bioenergetic View of Health

By focusing on how our bodies produce and use energy, we can determine how to best reverse energy deficiencies.

Energy is produced in the mitochondria, or “engines,” of our cells through a process called respiration. This process uses fuel from food, like carbohydrates and fats, along with other nutrients, like vitamins, minerals, and oxygen, to produce energy. This energy is held in a molecule called ATP.

(In future articles I’ll explore mitochondrial respiration more closely, including the differences between the oxidation of carbs and fats and other inputs that affect these processes.)

The energy produced from mitochondrial respiration is then used to perform all our functions. This includes our basic functions like breathing and keeping our heart beating, as well as maintaining our structure.

Energy is also used to handle stressors, which are any external energy demands. This includes physical activity, like exercise, and mental activity, like problem-solving and processing emotions, in addition to handling damage from things like infections, EMFs, or mold and detoxifying toxins like endotoxin.

In other words, this is why these various “causes” of different diseases aren’t independent from one another – they all exert their effects through a common means: depleting our energy supply.

When we don’t have enough energy to handle these stressors, perform our basic functions, and maintain our structure, we begin to have problems. The energy to handle these functions has to come from somewhere, and it typically comes from the maintenance and integrity of our structure. This causes deterioration over time and inhibits proper function, which eventually leads to the chronic conditions we see today in epidemic proportions.

In order to prevent this from happening and even reverse it, we have to improve mitochondrial respiration to produce more energy and reduce our stressors so that more energy is left to repair and maintain our structure.

 

The Many Dangers of Energy Deficiencies

We’ve already talked about how a lack of energy underlies the chronic conditions we’re seeing today in epidemic proportions, but energy affects all aspects of our health.

Because energy is the driving force behind all our functions and our entire structure, a lack of energy can result in all sorts of symptoms. This includes cold hands and feet or always feeling cold, fatigue, weight gain, muscle loss, hair loss, lack of libido, irritability and unstable mood, difficulty concentrating, weak hair and nails, hair loss, dry skin, insomnia, constant hunger or cravings, a lack of appetite, chronic infections, depression, PMS, headaches and migraines, swelling and edema, infertility, and many more common symptoms.

Virtually all of these symptoms were seen in the Minnesota Starvation Experiment, a study dedicated to figuring out what happens when we starve our bodies of energy (14). In this experiment, which was performed in the 1940s, participants were put on diets of around 1,800 calories per day for 6 months. This reduced-calorie diet isn’t too far off from commonly recommended fat-loss diets today, based on the participants’ height and weight.

The effects of this reduced-calorie diet were astounding, and completely changed the lives of the participants. Their health deteriorated to an incredible extent and they experienced all sorts of symptoms, including most of the ones mentioned above. It took between 2 months and 2 years of eating as much as 4,000-5,000 calories per day following the experiment for the participants to fully recover.

This experiment studied energy deficiency in the context of a low-calorie diet, which is a surefire way to reduce available energy. But, energy deficiencies are extraordinarily common nowadays even when consuming normal- or high-calorie diets.

Mitochondrial respiration, or energy production, can be inhibited by numerous factors, such as PUFA, nutrient deficiencies, and endotoxin. So even if we’re eating enough food, we still may not be converting it to usable energy. (This is what underlies fat gain, as I’ve explained in several articles.)

This is not even considering the excessive amounts of stressors that our bodies must use energy to handle, like psychological stress, environmental toxins, and EMFs.

Increasing our energy supply by improving mitochondrial respiration and reducing excessive energy demands is the key to resolving the more minor symptoms of energy deficiency, such as cold hands and feet, as well as the larger symptoms, like fat gain, infertility, and chronic conditions.

How exactly do we do that?

Well, this is the question.

And there’s not a simple answer.

This process is affected by pretty much everything in our internal and external environment, from the food we eat to the amount of sunlight we get. Of course, this can’t all be explained in one go, which is why energy is a theme that I come back to in pretty much every one of my articles.

Plus, there’s all sorts of ridiculousness out there when it comes to improving mitochondrial function, including completely misguided recommendations like ketogenic diets and fasting, which often steer people astray. I’ll cover these topics in future articles as well.

 

In the meantime, you can check out the free health and energy balance mini-course, which you can sign up for below! In this mini-course, I outline several of the more important factors affecting energy production and usage, how they affect our health, and what you can do about them.

 

References

It All Comes Down To Energy

Modern biology centers around a reductionist, mechanical view of the human body that permeates both conventional and alternative medicine.

Each bodily system is considered to be separate and independent from one another. The function of the heart is unrelated to the function of the brain which is unrelated to the function of the liver, and so on.

This leads to the treatment of symptoms, which has become the primary focus of conventional medicine. If cholesterol levels are high, a cholesterol-lowering drug is prescribed. If blood pressure is high, a blood-pressure-lowering drug is prescribed. If the immune system is overactive, an immunosuppressive-drug is prescribed.

And what’s considered to cause the modern epidemic of symptoms and diseases? Typically, the answer is genetics.

(It is becoming slightly more common to consider lifestyle factors as a minor contributor to some diseases, but there’s still very little focus on these factors.)

Alternative medicines often follow a similar path, where medications are substituted with “natural” supplements or other symptom-based treatments. While there may be slightly more emphasis on lifestyle factors, many people in the alternative medicine community are taking handfuls of supplements every day, each one for a different symptom.

Many other non-conventional medicines, like integrative and functional medicine, also fall into the same reductionist tendencies. They might not be as quick to prescribe medications or supplements and they may have more emphasis on lifestyle factors, but there’s still a focus on independent causes for various conditions.

In these forms of medicine, there’s often a wild goose chase for the cause of a symptom or condition. An endless search ensues to find some form of nutrient deficiency, hormonal imbalance, mold toxin exposure, EMF exposure, gut infection, heavy metal toxicity, or other environmental harm, with the solution being to remove that causative factor. They still miss that all of the problems and their causes fall under the same umbrella… energy.

 

Why Energy?

Energy is the driving force behind all our functions and our entire structure. As such, it also serves as the unifying principle that underlies our health.

Energy allows us to breathe, think, digest food, sleep, heal injuries, move, and just about anything else you can think of. It also maintains our structure, from the structure of every individual cell to the structure of our muscles, bones, organs, fascia, skin, hair, nails, and all our other tissues.

It’s therefore logical, but perhaps counterintuitive, that virtually any condition or symptom that we experience is due to a lack of energy, which inhibits proper function and structure.

That’s right, everything from fatigue to autoimmune conditions (1, 2, 3), diabetes and insulin resistance (4, 5, 6, 7), obesity (8), cancer (9), hypertension, allergies, fibromyalgia, neuropsychiatric and neurodegenerative conditions (10, 11, 12) like Alzheimer’s, Parkinson’s, ALS, multiple sclerosis, Huntington’s, depression, bipolar disorder, schizophrenia, and autism, and pretty much every other condition can be traced back to an energy deficiency (13).

So, it makes infinitely more sense to shift our focus away from the individual symptoms, conditions, and causes, and towards a bioenergetic view of health.

 

A Bioenergetic View of Health

By focusing on how our bodies produce and use energy, we can determine how to best reverse energy deficiencies.

Energy is produced in the mitochondria, or “engines,” of our cells through a process called respiration. This process uses fuel from food, like carbohydrates and fats, along with other nutrients, like vitamins, minerals, and oxygen, to produce energy. This energy is held in a molecule called ATP.

(In future articles I’ll explore mitochondrial respiration more closely, including the differences between the oxidation of carbs and fats and other inputs that affect these processes.)

The energy produced from mitochondrial respiration is then used to perform all our functions. This includes our basic functions like breathing and keeping our heart beating, as well as maintaining our structure.

Energy is also used to handle stressors, which are any external energy demands. This includes physical activity, like exercise, and mental activity, like problem-solving and processing emotions, in addition to handling damage from things like infections, EMFs, or mold and detoxifying toxins like endotoxin.

In other words, this is why these various “causes” of different diseases aren’t independent from one another – they all exert their effects through a common means: depleting our energy supply.

When we don’t have enough energy to handle these stressors, perform our basic functions, and maintain our structure, we begin to have problems. The energy to handle these functions has to come from somewhere, and it typically comes from the maintenance and integrity of our structure. This causes deterioration over time and inhibits proper function, which eventually leads to the chronic conditions we see today in epidemic proportions.

In order to prevent this from happening and even reverse it, we have to improve mitochondrial respiration to produce more energy and reduce our stressors so that more energy is left to repair and maintain our structure.

 

The Many Dangers of Energy Deficiencies

We’ve already talked about how a lack of energy underlies the chronic conditions we’re seeing today in epidemic proportions, but energy affects all aspects of our health.

Because energy is the driving force behind all our functions and our entire structure, a lack of energy can result in all sorts of symptoms. This includes cold hands and feet or always feeling cold, fatigue, weight gain, muscle loss, hair loss, lack of libido, irritability and unstable mood, difficulty concentrating, weak hair and nails, hair loss, dry skin, insomnia, constant hunger or cravings, a lack of appetite, chronic infections, depression, PMS, headaches and migraines, swelling and edema, infertility, and many more common symptoms.

Virtually all of these symptoms were seen in the Minnesota Starvation Experiment, a study dedicated to figuring out what happens when we starve our bodies of energy (14). In this experiment, which was performed in the 1940s, participants were put on diets of around 1,800 calories per day for 6 months. This reduced-calorie diet isn’t too far off from commonly recommended fat-loss diets today, based on the participants’ height and weight.

The effects of this reduced-calorie diet were astounding, and completely changed the lives of the participants. Their health deteriorated to an incredible extent and they experienced all sorts of symptoms, including most of the ones mentioned above. It took between 2 months and 2 years of eating as much as 4,000-5,000 calories per day following the experiment for the participants to fully recover.

This experiment studied energy deficiency in the context of a low-calorie diet, which is a surefire way to reduce available energy. But, energy deficiencies are extraordinarily common nowadays even when consuming normal- or high-calorie diets.

Mitochondrial respiration, or energy production, can be inhibited by numerous factors, such as PUFA, nutrient deficiencies, and endotoxin. So even if we’re eating enough food, we still may not be converting it to usable energy. (This is what underlies fat gain, as I’ve explained in several articles.)

This is not even considering the excessive amounts of stressors that our bodies must use energy to handle, like psychological stress, environmental toxins, and EMFs.

Increasing our energy supply by improving mitochondrial respiration and reducing excessive energy demands is the key to resolving the more minor symptoms of energy deficiency, such as cold hands and feet, as well as the larger symptoms, like fat gain, infertility, and chronic conditions.

How exactly do we do that?

Well, this is the question.

And there’s not a simple answer.

This process is affected by pretty much everything in our internal and external environment, from the food we eat to the amount of sunlight we get. Of course, this can’t all be explained in one go, which is why energy is a theme that I come back to in pretty much every one of my articles.

Plus, there’s all sorts of ridiculousness out there when it comes to improving mitochondrial function, including completely misguided recommendations like ketogenic diets and fasting, which often steer people astray. I’ll cover these topics in future articles as well.

 

In the meantime, you can check out the free health and energy balance mini-course, which you can sign up for below! In this mini-course, I outline several of the more important factors affecting energy production and usage, how they affect our health, and what you can do about them.

 

References

It All Comes Down To Energy

Modern biology centers around a reductionist, mechanical view of the human body that permeates both conventional and alternative medicine.

Each bodily system is considered to be separate and independent from one another. The function of the heart is unrelated to the function of the brain which is unrelated to the function of the liver, and so on.

This leads to the treatment of symptoms, which has become the primary focus of conventional medicine. If cholesterol levels are high, a cholesterol-lowering drug is prescribed. If blood pressure is high, a blood-pressure-lowering drug is prescribed. If the immune system is overactive, an immunosuppressive-drug is prescribed.

And what’s considered to cause the modern epidemic of symptoms and diseases? Typically, the answer is genetics.

(It is becoming slightly more common to consider lifestyle factors as a minor contributor to some diseases, but there’s still very little focus on these factors.)

Alternative medicines often follow a similar path, where medications are substituted with “natural” supplements or other symptom-based treatments. While there may be slightly more emphasis on lifestyle factors, many people in the alternative medicine community are taking handfuls of supplements every day, each one for a different symptom.

Many other non-conventional medicines, like integrative and functional medicine, also fall into the same reductionist tendencies. They might not be as quick to prescribe medications or supplements and they may have more emphasis on lifestyle factors, but there’s still a focus on independent causes for various conditions.

In these forms of medicine, there’s often a wild goose chase for the cause of a symptom or condition. An endless search ensues to find some form of nutrient deficiency, hormonal imbalance, mold toxin exposure, EMF exposure, gut infection, heavy metal toxicity, or other environmental harm, with the solution being to remove that causative factor. They still miss that all of the problems and their causes fall under the same umbrella… energy.

 

Why Energy?

Energy is the driving force behind all our functions and our entire structure. As such, it also serves as the unifying principle that underlies our health.

Energy allows us to breathe, think, digest food, sleep, heal injuries, move, and just about anything else you can think of. It also maintains our structure, from the structure of every individual cell to the structure of our muscles, bones, organs, fascia, skin, hair, nails, and all our other tissues.

It’s therefore logical, but perhaps counterintuitive, that virtually any condition or symptom that we experience is due to a lack of energy, which inhibits proper function and structure.

That’s right, everything from fatigue to autoimmune conditions (1, 2, 3), diabetes and insulin resistance (4, 5, 6, 7), obesity (8), cancer (9), hypertension, allergies, fibromyalgia, neuropsychiatric and neurodegenerative conditions (10, 11, 12) like Alzheimer’s, Parkinson’s, ALS, multiple sclerosis, Huntington’s, depression, bipolar disorder, schizophrenia, and autism, and pretty much every other condition can be traced back to an energy deficiency (13).

So, it makes infinitely more sense to shift our focus away from the individual symptoms, conditions, and causes, and towards a bioenergetic view of health.

 

A Bioenergetic View of Health

By focusing on how our bodies produce and use energy, we can determine how to best reverse energy deficiencies.

Energy is produced in the mitochondria, or “engines,” of our cells through a process called respiration. This process uses fuel from food, like carbohydrates and fats, along with other nutrients, like vitamins, minerals, and oxygen, to produce energy. This energy is held in a molecule called ATP.

(In future articles I’ll explore mitochondrial respiration more closely, including the differences between the oxidation of carbs and fats and other inputs that affect these processes.)

The energy produced from mitochondrial respiration is then used to perform all our functions. This includes our basic functions like breathing and keeping our heart beating, as well as maintaining our structure.

Energy is also used to handle stressors, which are any external energy demands. This includes physical activity, like exercise, and mental activity, like problem-solving and processing emotions, in addition to handling damage from things like infections, EMFs, or mold and detoxifying toxins like endotoxin.

In other words, this is why these various “causes” of different diseases aren’t independent from one another – they all exert their effects through a common means: depleting our energy supply.

When we don’t have enough energy to handle these stressors, perform our basic functions, and maintain our structure, we begin to have problems. The energy to handle these functions has to come from somewhere, and it typically comes from the maintenance and integrity of our structure. This causes deterioration over time and inhibits proper function, which eventually leads to the chronic conditions we see today in epidemic proportions.

In order to prevent this from happening and even reverse it, we have to improve mitochondrial respiration to produce more energy and reduce our stressors so that more energy is left to repair and maintain our structure.

 

The Many Dangers of Energy Deficiencies

We’ve already talked about how a lack of energy underlies the chronic conditions we’re seeing today in epidemic proportions, but energy affects all aspects of our health.

Because energy is the driving force behind all our functions and our entire structure, a lack of energy can result in all sorts of symptoms. This includes cold hands and feet or always feeling cold, fatigue, weight gain, muscle loss, hair loss, lack of libido, irritability and unstable mood, difficulty concentrating, weak hair and nails, hair loss, dry skin, insomnia, constant hunger or cravings, a lack of appetite, chronic infections, depression, PMS, headaches and migraines, swelling and edema, infertility, and many more common symptoms.

Virtually all of these symptoms were seen in the Minnesota Starvation Experiment, a study dedicated to figuring out what happens when we starve our bodies of energy (14). In this experiment, which was performed in the 1940s, participants were put on diets of around 1,800 calories per day for 6 months. This reduced-calorie diet isn’t too far off from commonly recommended fat-loss diets today, based on the participants’ height and weight.

The effects of this reduced-calorie diet were astounding, and completely changed the lives of the participants. Their health deteriorated to an incredible extent and they experienced all sorts of symptoms, including most of the ones mentioned above. It took between 2 months and 2 years of eating as much as 4,000-5,000 calories per day following the experiment for the participants to fully recover.

This experiment studied energy deficiency in the context of a low-calorie diet, which is a surefire way to reduce available energy. But, energy deficiencies are extraordinarily common nowadays even when consuming normal- or high-calorie diets.

Mitochondrial respiration, or energy production, can be inhibited by numerous factors, such as PUFA, nutrient deficiencies, and endotoxin. So even if we’re eating enough food, we still may not be converting it to usable energy. (This is what underlies fat gain, as I’ve explained in several articles.)

This is not even considering the excessive amounts of stressors that our bodies must use energy to handle, like psychological stress, environmental toxins, and EMFs.

Increasing our energy supply by improving mitochondrial respiration and reducing excessive energy demands is the key to resolving the more minor symptoms of energy deficiency, such as cold hands and feet, as well as the larger symptoms, like fat gain, infertility, and chronic conditions.

How exactly do we do that?

Well, this is the question.

And there’s not a simple answer.

This process is affected by pretty much everything in our internal and external environment, from the food we eat to the amount of sunlight we get. Of course, this can’t all be explained in one go, which is why energy is a theme that I come back to in pretty much every one of my articles.

Plus, there’s all sorts of ridiculousness out there when it comes to improving mitochondrial function, including completely misguided recommendations like ketogenic diets and fasting, which often steer people astray. I’ll cover these topics in future articles as well.

 

In the meantime, you can check out the free health and energy balance mini-course, which you can sign up for below! In this mini-course, I outline several of the more important factors affecting energy production and usage, how they affect our health, and what you can do about them.

 

References

It All Comes Down To Energy

Modern biology centers around a reductionist, mechanical view of the human body that permeates both conventional and alternative medicine.

Each bodily system is considered to be separate and independent from one another. The function of the heart is unrelated to the function of the brain which is unrelated to the function of the liver, and so on.

This leads to the treatment of symptoms, which has become the primary focus of conventional medicine. If cholesterol levels are high, a cholesterol-lowering drug is prescribed. If blood pressure is high, a blood-pressure-lowering drug is prescribed. If the immune system is overactive, an immunosuppressive-drug is prescribed.

And what’s considered to cause the modern epidemic of symptoms and diseases? Typically, the answer is genetics.

(It is becoming slightly more common to consider lifestyle factors as a minor contributor to some diseases, but there’s still very little focus on these factors.)

Alternative medicines often follow a similar path, where medications are substituted with “natural” supplements or other symptom-based treatments. While there may be slightly more emphasis on lifestyle factors, many people in the alternative medicine community are taking handfuls of supplements every day, each one for a different symptom.

Many other non-conventional medicines, like integrative and functional medicine, also fall into the same reductionist tendencies. They might not be as quick to prescribe medications or supplements and they may have more emphasis on lifestyle factors, but there’s still a focus on independent causes for various conditions.

In these forms of medicine, there’s often a wild goose chase for the cause of a symptom or condition. An endless search ensues to find some form of nutrient deficiency, hormonal imbalance, mold toxin exposure, EMF exposure, gut infection, heavy metal toxicity, or other environmental harm, with the solution being to remove that causative factor. They still miss that all of the problems and their causes fall under the same umbrella… energy.

 

Why Energy?

Energy is the driving force behind all our functions and our entire structure. As such, it also serves as the unifying principle that underlies our health.

Energy allows us to breathe, think, digest food, sleep, heal injuries, move, and just about anything else you can think of. It also maintains our structure, from the structure of every individual cell to the structure of our muscles, bones, organs, fascia, skin, hair, nails, and all our other tissues.

It’s therefore logical, but perhaps counterintuitive, that virtually any condition or symptom that we experience is due to a lack of energy, which inhibits proper function and structure.

That’s right, everything from fatigue to autoimmune conditions (1, 2, 3), diabetes and insulin resistance (4, 5, 6, 7), obesity (8), cancer (9), hypertension, allergies, fibromyalgia, neuropsychiatric and neurodegenerative conditions (10, 11, 12) like Alzheimer’s, Parkinson’s, ALS, multiple sclerosis, Huntington’s, depression, bipolar disorder, schizophrenia, and autism, and pretty much every other condition can be traced back to an energy deficiency (13).

So, it makes infinitely more sense to shift our focus away from the individual symptoms, conditions, and causes, and towards a bioenergetic view of health.

 

A Bioenergetic View of Health

By focusing on how our bodies produce and use energy, we can determine how to best reverse energy deficiencies.

Energy is produced in the mitochondria, or “engines,” of our cells through a process called respiration. This process uses fuel from food, like carbohydrates and fats, along with other nutrients, like vitamins, minerals, and oxygen, to produce energy. This energy is held in a molecule called ATP.

(In future articles I’ll explore mitochondrial respiration more closely, including the differences between the oxidation of carbs and fats and other inputs that affect these processes.)

The energy produced from mitochondrial respiration is then used to perform all our functions. This includes our basic functions like breathing and keeping our heart beating, as well as maintaining our structure.

Energy is also used to handle stressors, which are any external energy demands. This includes physical activity, like exercise, and mental activity, like problem-solving and processing emotions, in addition to handling damage from things like infections, EMFs, or mold and detoxifying toxins like endotoxin.

In other words, this is why these various “causes” of different diseases aren’t independent from one another – they all exert their effects through a common means: depleting our energy supply.

When we don’t have enough energy to handle these stressors, perform our basic functions, and maintain our structure, we begin to have problems. The energy to handle these functions has to come from somewhere, and it typically comes from the maintenance and integrity of our structure. This causes deterioration over time and inhibits proper function, which eventually leads to the chronic conditions we see today in epidemic proportions.

In order to prevent this from happening and even reverse it, we have to improve mitochondrial respiration to produce more energy and reduce our stressors so that more energy is left to repair and maintain our structure.

 

The Many Dangers of Energy Deficiencies

We’ve already talked about how a lack of energy underlies the chronic conditions we’re seeing today in epidemic proportions, but energy affects all aspects of our health.

Because energy is the driving force behind all our functions and our entire structure, a lack of energy can result in all sorts of symptoms. This includes cold hands and feet or always feeling cold, fatigue, weight gain, muscle loss, hair loss, lack of libido, irritability and unstable mood, difficulty concentrating, weak hair and nails, hair loss, dry skin, insomnia, constant hunger or cravings, a lack of appetite, chronic infections, depression, PMS, headaches and migraines, swelling and edema, infertility, and many more common symptoms.

Virtually all of these symptoms were seen in the Minnesota Starvation Experiment, a study dedicated to figuring out what happens when we starve our bodies of energy (14). In this experiment, which was performed in the 1940s, participants were put on diets of around 1,800 calories per day for 6 months. This reduced-calorie diet isn’t too far off from commonly recommended fat-loss diets today, based on the participants’ height and weight.

The effects of this reduced-calorie diet were astounding, and completely changed the lives of the participants. Their health deteriorated to an incredible extent and they experienced all sorts of symptoms, including most of the ones mentioned above. It took between 2 months and 2 years of eating as much as 4,000-5,000 calories per day following the experiment for the participants to fully recover.

This experiment studied energy deficiency in the context of a low-calorie diet, which is a surefire way to reduce available energy. But, energy deficiencies are extraordinarily common nowadays even when consuming normal- or high-calorie diets.

Mitochondrial respiration, or energy production, can be inhibited by numerous factors, such as PUFA, nutrient deficiencies, and endotoxin. So even if we’re eating enough food, we still may not be converting it to usable energy. (This is what underlies fat gain, as I’ve explained in several articles.)

This is not even considering the excessive amounts of stressors that our bodies must use energy to handle, like psychological stress, environmental toxins, and EMFs.

Increasing our energy supply by improving mitochondrial respiration and reducing excessive energy demands is the key to resolving the more minor symptoms of energy deficiency, such as cold hands and feet, as well as the larger symptoms, like fat gain, infertility, and chronic conditions.

How exactly do we do that?

Well, this is the question.

And there’s not a simple answer.

This process is affected by pretty much everything in our internal and external environment, from the food we eat to the amount of sunlight we get. Of course, this can’t all be explained in one go, which is why energy is a theme that I come back to in pretty much every one of my articles.

Plus, there’s all sorts of ridiculousness out there when it comes to improving mitochondrial function, including completely misguided recommendations like ketogenic diets and fasting, which often steer people astray. I’ll cover these topics in future articles as well.

 

In the meantime, you can check out the free health and energy balance mini-course, which you can sign up for below! In this mini-course, I outline several of the more important factors affecting energy production and usage, how they affect our health, and what you can do about them.

 

References

It All Comes Down To Energy

Modern biology centers around a reductionist, mechanical view of the human body that permeates both conventional and alternative medicine.

Each bodily system is considered to be separate and independent from one another. The function of the heart is unrelated to the function of the brain which is unrelated to the function of the liver, and so on.

This leads to the treatment of symptoms, which has become the primary focus of conventional medicine. If cholesterol levels are high, a cholesterol-lowering drug is prescribed. If blood pressure is high, a blood-pressure-lowering drug is prescribed. If the immune system is overactive, an immunosuppressive-drug is prescribed.

And what’s considered to cause the modern epidemic of symptoms and diseases? Typically, the answer is genetics.

(It is becoming slightly more common to consider lifestyle factors as a minor contributor to some diseases, but there’s still very little focus on these factors.)

Alternative medicines often follow a similar path, where medications are substituted with “natural” supplements or other symptom-based treatments. While there may be slightly more emphasis on lifestyle factors, many people in the alternative medicine community are taking handfuls of supplements every day, each one for a different symptom.

Many other non-conventional medicines, like integrative and functional medicine, also fall into the same reductionist tendencies. They might not be as quick to prescribe medications or supplements and they may have more emphasis on lifestyle factors, but there’s still a focus on independent causes for various conditions.

In these forms of medicine, there’s often a wild goose chase for the cause of a symptom or condition. An endless search ensues to find some form of nutrient deficiency, hormonal imbalance, mold toxin exposure, EMF exposure, gut infection, heavy metal toxicity, or other environmental harm, with the solution being to remove that causative factor. They still miss that all of the problems and their causes fall under the same umbrella… energy.

 

Why Energy?

Energy is the driving force behind all our functions and our entire structure. As such, it also serves as the unifying principle that underlies our health.

Energy allows us to breathe, think, digest food, sleep, heal injuries, move, and just about anything else you can think of. It also maintains our structure, from the structure of every individual cell to the structure of our muscles, bones, organs, fascia, skin, hair, nails, and all our other tissues.

It’s therefore logical, but perhaps counterintuitive, that virtually any condition or symptom that we experience is due to a lack of energy, which inhibits proper function and structure.

That’s right, everything from fatigue to autoimmune conditions (1, 2, 3), diabetes and insulin resistance (4, 5, 6, 7), obesity (8), cancer (9), hypertension, allergies, fibromyalgia, neuropsychiatric and neurodegenerative conditions (10, 11, 12) like Alzheimer’s, Parkinson’s, ALS, multiple sclerosis, Huntington’s, depression, bipolar disorder, schizophrenia, and autism, and pretty much every other condition can be traced back to an energy deficiency (13).

So, it makes infinitely more sense to shift our focus away from the individual symptoms, conditions, and causes, and towards a bioenergetic view of health.

 

A Bioenergetic View of Health

By focusing on how our bodies produce and use energy, we can determine how to best reverse energy deficiencies.

Energy is produced in the mitochondria, or “engines,” of our cells through a process called respiration. This process uses fuel from food, like carbohydrates and fats, along with other nutrients, like vitamins, minerals, and oxygen, to produce energy. This energy is held in a molecule called ATP.

(In future articles I’ll explore mitochondrial respiration more closely, including the differences between the oxidation of carbs and fats and other inputs that affect these processes.)

The energy produced from mitochondrial respiration is then used to perform all our functions. This includes our basic functions like breathing and keeping our heart beating, as well as maintaining our structure.

Energy is also used to handle stressors, which are any external energy demands. This includes physical activity, like exercise, and mental activity, like problem-solving and processing emotions, in addition to handling damage from things like infections, EMFs, or mold and detoxifying toxins like endotoxin.

In other words, this is why these various “causes” of different diseases aren’t independent from one another – they all exert their effects through a common means: depleting our energy supply.

When we don’t have enough energy to handle these stressors, perform our basic functions, and maintain our structure, we begin to have problems. The energy to handle these functions has to come from somewhere, and it typically comes from the maintenance and integrity of our structure. This causes deterioration over time and inhibits proper function, which eventually leads to the chronic conditions we see today in epidemic proportions.

In order to prevent this from happening and even reverse it, we have to improve mitochondrial respiration to produce more energy and reduce our stressors so that more energy is left to repair and maintain our structure.

 

The Many Dangers of Energy Deficiencies

We’ve already talked about how a lack of energy underlies the chronic conditions we’re seeing today in epidemic proportions, but energy affects all aspects of our health.

Because energy is the driving force behind all our functions and our entire structure, a lack of energy can result in all sorts of symptoms. This includes cold hands and feet or always feeling cold, fatigue, weight gain, muscle loss, hair loss, lack of libido, irritability and unstable mood, difficulty concentrating, weak hair and nails, hair loss, dry skin, insomnia, constant hunger or cravings, a lack of appetite, chronic infections, depression, PMS, headaches and migraines, swelling and edema, infertility, and many more common symptoms.

Virtually all of these symptoms were seen in the Minnesota Starvation Experiment, a study dedicated to figuring out what happens when we starve our bodies of energy (14). In this experiment, which was performed in the 1940s, participants were put on diets of around 1,800 calories per day for 6 months. This reduced-calorie diet isn’t too far off from commonly recommended fat-loss diets today, based on the participants’ height and weight.

The effects of this reduced-calorie diet were astounding, and completely changed the lives of the participants. Their health deteriorated to an incredible extent and they experienced all sorts of symptoms, including most of the ones mentioned above. It took between 2 months and 2 years of eating as much as 4,000-5,000 calories per day following the experiment for the participants to fully recover.

This experiment studied energy deficiency in the context of a low-calorie diet, which is a surefire way to reduce available energy. But, energy deficiencies are extraordinarily common nowadays even when consuming normal- or high-calorie diets.

Mitochondrial respiration, or energy production, can be inhibited by numerous factors, such as PUFA, nutrient deficiencies, and endotoxin. So even if we’re eating enough food, we still may not be converting it to usable energy. (This is what underlies fat gain, as I’ve explained in several articles.)

This is not even considering the excessive amounts of stressors that our bodies must use energy to handle, like psychological stress, environmental toxins, and EMFs.

Increasing our energy supply by improving mitochondrial respiration and reducing excessive energy demands is the key to resolving the more minor symptoms of energy deficiency, such as cold hands and feet, as well as the larger symptoms, like fat gain, infertility, and chronic conditions.

How exactly do we do that?

Well, this is the question.

And there’s not a simple answer.

This process is affected by pretty much everything in our internal and external environment, from the food we eat to the amount of sunlight we get. Of course, this can’t all be explained in one go, which is why energy is a theme that I come back to in pretty much every one of my articles.

Plus, there’s all sorts of ridiculousness out there when it comes to improving mitochondrial function, including completely misguided recommendations like ketogenic diets and fasting, which often steer people astray. I’ll cover these topics in future articles as well.

 

In the meantime, you can check out the free health and energy balance mini-course, which you can sign up for below! In this mini-course, I outline several of the more important factors affecting energy production and usage, how they affect our health, and what you can do about them.

 

References

It All Comes Down To Energy

Modern biology centers around a reductionist, mechanical view of the human body that permeates both conventional and alternative medicine.

Each bodily system is considered to be separate and independent from one another. The function of the heart is unrelated to the function of the brain which is unrelated to the function of the liver, and so on.

This leads to the treatment of symptoms, which has become the primary focus of conventional medicine. If cholesterol levels are high, a cholesterol-lowering drug is prescribed. If blood pressure is high, a blood-pressure-lowering drug is prescribed. If the immune system is overactive, an immunosuppressive-drug is prescribed.

And what’s considered to cause the modern epidemic of symptoms and diseases? Typically, the answer is genetics.

(It is becoming slightly more common to consider lifestyle factors as a minor contributor to some diseases, but there’s still very little focus on these factors.)

Alternative medicines often follow a similar path, where medications are substituted with “natural” supplements or other symptom-based treatments. While there may be slightly more emphasis on lifestyle factors, many people in the alternative medicine community are taking handfuls of supplements every day, each one for a different symptom.

Many other non-conventional medicines, like integrative and functional medicine, also fall into the same reductionist tendencies. They might not be as quick to prescribe medications or supplements and they may have more emphasis on lifestyle factors, but there’s still a focus on independent causes for various conditions.

In these forms of medicine, there’s often a wild goose chase for the cause of a symptom or condition. An endless search ensues to find some form of nutrient deficiency, hormonal imbalance, mold toxin exposure, EMF exposure, gut infection, heavy metal toxicity, or other environmental harm, with the solution being to remove that causative factor. They still miss that all of the problems and their causes fall under the same umbrella… energy.

 

Why Energy?

Energy is the driving force behind all our functions and our entire structure. As such, it also serves as the unifying principle that underlies our health.

Energy allows us to breathe, think, digest food, sleep, heal injuries, move, and just about anything else you can think of. It also maintains our structure, from the structure of every individual cell to the structure of our muscles, bones, organs, fascia, skin, hair, nails, and all our other tissues.

It’s therefore logical, but perhaps counterintuitive, that virtually any condition or symptom that we experience is due to a lack of energy, which inhibits proper function and structure.

That’s right, everything from fatigue to autoimmune conditions (1, 2, 3), diabetes and insulin resistance (4, 5, 6, 7), obesity (8), cancer (9), hypertension, allergies, fibromyalgia, neuropsychiatric and neurodegenerative conditions (10, 11, 12) like Alzheimer’s, Parkinson’s, ALS, multiple sclerosis, Huntington’s, depression, bipolar disorder, schizophrenia, and autism, and pretty much every other condition can be traced back to an energy deficiency (13).

So, it makes infinitely more sense to shift our focus away from the individual symptoms, conditions, and causes, and towards a bioenergetic view of health.

 

A Bioenergetic View of Health

By focusing on how our bodies produce and use energy, we can determine how to best reverse energy deficiencies.

Energy is produced in the mitochondria, or “engines,” of our cells through a process called respiration. This process uses fuel from food, like carbohydrates and fats, along with other nutrients, like vitamins, minerals, and oxygen, to produce energy. This energy is held in a molecule called ATP.

(In future articles I’ll explore mitochondrial respiration more closely, including the differences between the oxidation of carbs and fats and other inputs that affect these processes.)

The energy produced from mitochondrial respiration is then used to perform all our functions. This includes our basic functions like breathing and keeping our heart beating, as well as maintaining our structure.

Energy is also used to handle stressors, which are any external energy demands. This includes physical activity, like exercise, and mental activity, like problem-solving and processing emotions, in addition to handling damage from things like infections, EMFs, or mold and detoxifying toxins like endotoxin.

In other words, this is why these various “causes” of different diseases aren’t independent from one another – they all exert their effects through a common means: depleting our energy supply.

When we don’t have enough energy to handle these stressors, perform our basic functions, and maintain our structure, we begin to have problems. The energy to handle these functions has to come from somewhere, and it typically comes from the maintenance and integrity of our structure. This causes deterioration over time and inhibits proper function, which eventually leads to the chronic conditions we see today in epidemic proportions.

In order to prevent this from happening and even reverse it, we have to improve mitochondrial respiration to produce more energy and reduce our stressors so that more energy is left to repair and maintain our structure.

 

The Many Dangers of Energy Deficiencies

We’ve already talked about how a lack of energy underlies the chronic conditions we’re seeing today in epidemic proportions, but energy affects all aspects of our health.

Because energy is the driving force behind all our functions and our entire structure, a lack of energy can result in all sorts of symptoms. This includes cold hands and feet or always feeling cold, fatigue, weight gain, muscle loss, hair loss, lack of libido, irritability and unstable mood, difficulty concentrating, weak hair and nails, hair loss, dry skin, insomnia, constant hunger or cravings, a lack of appetite, chronic infections, depression, PMS, headaches and migraines, swelling and edema, infertility, and many more common symptoms.

Virtually all of these symptoms were seen in the Minnesota Starvation Experiment, a study dedicated to figuring out what happens when we starve our bodies of energy (14). In this experiment, which was performed in the 1940s, participants were put on diets of around 1,800 calories per day for 6 months. This reduced-calorie diet isn’t too far off from commonly recommended fat-loss diets today, based on the participants’ height and weight.

The effects of this reduced-calorie diet were astounding, and completely changed the lives of the participants. Their health deteriorated to an incredible extent and they experienced all sorts of symptoms, including most of the ones mentioned above. It took between 2 months and 2 years of eating as much as 4,000-5,000 calories per day following the experiment for the participants to fully recover.

This experiment studied energy deficiency in the context of a low-calorie diet, which is a surefire way to reduce available energy. But, energy deficiencies are extraordinarily common nowadays even when consuming normal- or high-calorie diets.

Mitochondrial respiration, or energy production, can be inhibited by numerous factors, such as PUFA, nutrient deficiencies, and endotoxin. So even if we’re eating enough food, we still may not be converting it to usable energy. (This is what underlies fat gain, as I’ve explained in several articles.)

This is not even considering the excessive amounts of stressors that our bodies must use energy to handle, like psychological stress, environmental toxins, and EMFs.

Increasing our energy supply by improving mitochondrial respiration and reducing excessive energy demands is the key to resolving the more minor symptoms of energy deficiency, such as cold hands and feet, as well as the larger symptoms, like fat gain, infertility, and chronic conditions.

How exactly do we do that?

Well, this is the question.

And there’s not a simple answer.

This process is affected by pretty much everything in our internal and external environment, from the food we eat to the amount of sunlight we get. Of course, this can’t all be explained in one go, which is why energy is a theme that I come back to in pretty much every one of my articles.

Plus, there’s all sorts of ridiculousness out there when it comes to improving mitochondrial function, including completely misguided recommendations like ketogenic diets and fasting, which often steer people astray. I’ll cover these topics in future articles as well.

 

In the meantime, you can check out the free health and energy balance mini-course, which you can sign up for below! In this mini-course, I outline several of the more important factors affecting energy production and usage, how they affect our health, and what you can do about them.

 

References

It All Comes Down To Energy

Modern biology centers around a reductionist, mechanical view of the human body that permeates both conventional and alternative medicine.

Each bodily system is considered to be separate and independent from one another. The function of the heart is unrelated to the function of the brain which is unrelated to the function of the liver, and so on.

This leads to the treatment of symptoms, which has become the primary focus of conventional medicine. If cholesterol levels are high, a cholesterol-lowering drug is prescribed. If blood pressure is high, a blood-pressure-lowering drug is prescribed. If the immune system is overactive, an immunosuppressive-drug is prescribed.

And what’s considered to cause the modern epidemic of symptoms and diseases? Typically, the answer is genetics.

(It is becoming slightly more common to consider lifestyle factors as a minor contributor to some diseases, but there’s still very little focus on these factors.)

Alternative medicines often follow a similar path, where medications are substituted with “natural” supplements or other symptom-based treatments. While there may be slightly more emphasis on lifestyle factors, many people in the alternative medicine community are taking handfuls of supplements every day, each one for a different symptom.

Many other non-conventional medicines, like integrative and functional medicine, also fall into the same reductionist tendencies. They might not be as quick to prescribe medications or supplements and they may have more emphasis on lifestyle factors, but there’s still a focus on independent causes for various conditions.

In these forms of medicine, there’s often a wild goose chase for the cause of a symptom or condition. An endless search ensues to find some form of nutrient deficiency, hormonal imbalance, mold toxin exposure, EMF exposure, gut infection, heavy metal toxicity, or other environmental harm, with the solution being to remove that causative factor. They still miss that all of the problems and their causes fall under the same umbrella… energy.

 

Why Energy?

Energy is the driving force behind all our functions and our entire structure. As such, it also serves as the unifying principle that underlies our health.

Energy allows us to breathe, think, digest food, sleep, heal injuries, move, and just about anything else you can think of. It also maintains our structure, from the structure of every individual cell to the structure of our muscles, bones, organs, fascia, skin, hair, nails, and all our other tissues.

It’s therefore logical, but perhaps counterintuitive, that virtually any condition or symptom that we experience is due to a lack of energy, which inhibits proper function and structure.

That’s right, everything from fatigue to autoimmune conditions (1, 2, 3), diabetes and insulin resistance (4, 5, 6, 7), obesity (8), cancer (9), hypertension, allergies, fibromyalgia, neuropsychiatric and neurodegenerative conditions (10, 11, 12) like Alzheimer’s, Parkinson’s, ALS, multiple sclerosis, Huntington’s, depression, bipolar disorder, schizophrenia, and autism, and pretty much every other condition can be traced back to an energy deficiency (13).

So, it makes infinitely more sense to shift our focus away from the individual symptoms, conditions, and causes, and towards a bioenergetic view of health.

 

A Bioenergetic View of Health

By focusing on how our bodies produce and use energy, we can determine how to best reverse energy deficiencies.

Energy is produced in the mitochondria, or “engines,” of our cells through a process called respiration. This process uses fuel from food, like carbohydrates and fats, along with other nutrients, like vitamins, minerals, and oxygen, to produce energy. This energy is held in a molecule called ATP.

(In future articles I’ll explore mitochondrial respiration more closely, including the differences between the oxidation of carbs and fats and other inputs that affect these processes.)

The energy produced from mitochondrial respiration is then used to perform all our functions. This includes our basic functions like breathing and keeping our heart beating, as well as maintaining our structure.

Energy is also used to handle stressors, which are any external energy demands. This includes physical activity, like exercise, and mental activity, like problem-solving and processing emotions, in addition to handling damage from things like infections, EMFs, or mold and detoxifying toxins like endotoxin.

In other words, this is why these various “causes” of different diseases aren’t independent from one another – they all exert their effects through a common means: depleting our energy supply.

When we don’t have enough energy to handle these stressors, perform our basic functions, and maintain our structure, we begin to have problems. The energy to handle these functions has to come from somewhere, and it typically comes from the maintenance and integrity of our structure. This causes deterioration over time and inhibits proper function, which eventually leads to the chronic conditions we see today in epidemic proportions.

In order to prevent this from happening and even reverse it, we have to improve mitochondrial respiration to produce more energy and reduce our stressors so that more energy is left to repair and maintain our structure.

 

The Many Dangers of Energy Deficiencies

We’ve already talked about how a lack of energy underlies the chronic conditions we’re seeing today in epidemic proportions, but energy affects all aspects of our health.

Because energy is the driving force behind all our functions and our entire structure, a lack of energy can result in all sorts of symptoms. This includes cold hands and feet or always feeling cold, fatigue, weight gain, muscle loss, hair loss, lack of libido, irritability and unstable mood, difficulty concentrating, weak hair and nails, hair loss, dry skin, insomnia, constant hunger or cravings, a lack of appetite, chronic infections, depression, PMS, headaches and migraines, swelling and edema, infertility, and many more common symptoms.

Virtually all of these symptoms were seen in the Minnesota Starvation Experiment, a study dedicated to figuring out what happens when we starve our bodies of energy (14). In this experiment, which was performed in the 1940s, participants were put on diets of around 1,800 calories per day for 6 months. This reduced-calorie diet isn’t too far off from commonly recommended fat-loss diets today, based on the participants’ height and weight.

The effects of this reduced-calorie diet were astounding, and completely changed the lives of the participants. Their health deteriorated to an incredible extent and they experienced all sorts of symptoms, including most of the ones mentioned above. It took between 2 months and 2 years of eating as much as 4,000-5,000 calories per day following the experiment for the participants to fully recover.

This experiment studied energy deficiency in the context of a low-calorie diet, which is a surefire way to reduce available energy. But, energy deficiencies are extraordinarily common nowadays even when consuming normal- or high-calorie diets.

Mitochondrial respiration, or energy production, can be inhibited by numerous factors, such as PUFA, nutrient deficiencies, and endotoxin. So even if we’re eating enough food, we still may not be converting it to usable energy. (This is what underlies fat gain, as I’ve explained in several articles.)

This is not even considering the excessive amounts of stressors that our bodies must use energy to handle, like psychological stress, environmental toxins, and EMFs.

Increasing our energy supply by improving mitochondrial respiration and reducing excessive energy demands is the key to resolving the more minor symptoms of energy deficiency, such as cold hands and feet, as well as the larger symptoms, like fat gain, infertility, and chronic conditions.

How exactly do we do that?

Well, this is the question.

And there’s not a simple answer.

This process is affected by pretty much everything in our internal and external environment, from the food we eat to the amount of sunlight we get. Of course, this can’t all be explained in one go, which is why energy is a theme that I come back to in pretty much every one of my articles.

Plus, there’s all sorts of ridiculousness out there when it comes to improving mitochondrial function, including completely misguided recommendations like ketogenic diets and fasting, which often steer people astray. I’ll cover these topics in future articles as well.

 

In the meantime, you can check out the free health and energy balance mini-course, which you can sign up for below! In this mini-course, I outline several of the more important factors affecting energy production and usage, how they affect our health, and what you can do about them.

 

References

It All Comes Down To Energy

Modern biology centers around a reductionist, mechanical view of the human body that permeates both conventional and alternative medicine.

Each bodily system is considered to be separate and independent from one another. The function of the heart is unrelated to the function of the brain which is unrelated to the function of the liver, and so on.

This leads to the treatment of symptoms, which has become the primary focus of conventional medicine. If cholesterol levels are high, a cholesterol-lowering drug is prescribed. If blood pressure is high, a blood-pressure-lowering drug is prescribed. If the immune system is overactive, an immunosuppressive-drug is prescribed.

And what’s considered to cause the modern epidemic of symptoms and diseases? Typically, the answer is genetics.

(It is becoming slightly more common to consider lifestyle factors as a minor contributor to some diseases, but there’s still very little focus on these factors.)

Alternative medicines often follow a similar path, where medications are substituted with “natural” supplements or other symptom-based treatments. While there may be slightly more emphasis on lifestyle factors, many people in the alternative medicine community are taking handfuls of supplements every day, each one for a different symptom.

Many other non-conventional medicines, like integrative and functional medicine, also fall into the same reductionist tendencies. They might not be as quick to prescribe medications or supplements and they may have more emphasis on lifestyle factors, but there’s still a focus on independent causes for various conditions.

In these forms of medicine, there’s often a wild goose chase for the cause of a symptom or condition. An endless search ensues to find some form of nutrient deficiency, hormonal imbalance, mold toxin exposure, EMF exposure, gut infection, heavy metal toxicity, or other environmental harm, with the solution being to remove that causative factor. They still miss that all of the problems and their causes fall under the same umbrella… energy.

 

Why Energy?

Energy is the driving force behind all our functions and our entire structure. As such, it also serves as the unifying principle that underlies our health.

Energy allows us to breathe, think, digest food, sleep, heal injuries, move, and just about anything else you can think of. It also maintains our structure, from the structure of every individual cell to the structure of our muscles, bones, organs, fascia, skin, hair, nails, and all our other tissues.

It’s therefore logical, but perhaps counterintuitive, that virtually any condition or symptom that we experience is due to a lack of energy, which inhibits proper function and structure.

That’s right, everything from fatigue to autoimmune conditions (1, 2, 3), diabetes and insulin resistance (4, 5, 6, 7), obesity (8), cancer (9), hypertension, allergies, fibromyalgia, neuropsychiatric and neurodegenerative conditions (10, 11, 12) like Alzheimer’s, Parkinson’s, ALS, multiple sclerosis, Huntington’s, depression, bipolar disorder, schizophrenia, and autism, and pretty much every other condition can be traced back to an energy deficiency (13).

So, it makes infinitely more sense to shift our focus away from the individual symptoms, conditions, and causes, and towards a bioenergetic view of health.

 

A Bioenergetic View of Health

By focusing on how our bodies produce and use energy, we can determine how to best reverse energy deficiencies.

Energy is produced in the mitochondria, or “engines,” of our cells through a process called respiration. This process uses fuel from food, like carbohydrates and fats, along with other nutrients, like vitamins, minerals, and oxygen, to produce energy. This energy is held in a molecule called ATP.

(In future articles I’ll explore mitochondrial respiration more closely, including the differences between the oxidation of carbs and fats and other inputs that affect these processes.)

The energy produced from mitochondrial respiration is then used to perform all our functions. This includes our basic functions like breathing and keeping our heart beating, as well as maintaining our structure.

Energy is also used to handle stressors, which are any external energy demands. This includes physical activity, like exercise, and mental activity, like problem-solving and processing emotions, in addition to handling damage from things like infections, EMFs, or mold and detoxifying toxins like endotoxin.

In other words, this is why these various “causes” of different diseases aren’t independent from one another – they all exert their effects through a common means: depleting our energy supply.

When we don’t have enough energy to handle these stressors, perform our basic functions, and maintain our structure, we begin to have problems. The energy to handle these functions has to come from somewhere, and it typically comes from the maintenance and integrity of our structure. This causes deterioration over time and inhibits proper function, which eventually leads to the chronic conditions we see today in epidemic proportions.

In order to prevent this from happening and even reverse it, we have to improve mitochondrial respiration to produce more energy and reduce our stressors so that more energy is left to repair and maintain our structure.

 

The Many Dangers of Energy Deficiencies

We’ve already talked about how a lack of energy underlies the chronic conditions we’re seeing today in epidemic proportions, but energy affects all aspects of our health.

Because energy is the driving force behind all our functions and our entire structure, a lack of energy can result in all sorts of symptoms. This includes cold hands and feet or always feeling cold, fatigue, weight gain, muscle loss, hair loss, lack of libido, irritability and unstable mood, difficulty concentrating, weak hair and nails, hair loss, dry skin, insomnia, constant hunger or cravings, a lack of appetite, chronic infections, depression, PMS, headaches and migraines, swelling and edema, infertility, and many more common symptoms.

Virtually all of these symptoms were seen in the Minnesota Starvation Experiment, a study dedicated to figuring out what happens when we starve our bodies of energy (14). In this experiment, which was performed in the 1940s, participants were put on diets of around 1,800 calories per day for 6 months. This reduced-calorie diet isn’t too far off from commonly recommended fat-loss diets today, based on the participants’ height and weight.

The effects of this reduced-calorie diet were astounding, and completely changed the lives of the participants. Their health deteriorated to an incredible extent and they experienced all sorts of symptoms, including most of the ones mentioned above. It took between 2 months and 2 years of eating as much as 4,000-5,000 calories per day following the experiment for the participants to fully recover.

This experiment studied energy deficiency in the context of a low-calorie diet, which is a surefire way to reduce available energy. But, energy deficiencies are extraordinarily common nowadays even when consuming normal- or high-calorie diets.

Mitochondrial respiration, or energy production, can be inhibited by numerous factors, such as PUFA, nutrient deficiencies, and endotoxin. So even if we’re eating enough food, we still may not be converting it to usable energy. (This is what underlies fat gain, as I’ve explained in several articles.)

This is not even considering the excessive amounts of stressors that our bodies must use energy to handle, like psychological stress, environmental toxins, and EMFs.

Increasing our energy supply by improving mitochondrial respiration and reducing excessive energy demands is the key to resolving the more minor symptoms of energy deficiency, such as cold hands and feet, as well as the larger symptoms, like fat gain, infertility, and chronic conditions.

How exactly do we do that?

Well, this is the question.

And there’s not a simple answer.

This process is affected by pretty much everything in our internal and external environment, from the food we eat to the amount of sunlight we get. Of course, this can’t all be explained in one go, which is why energy is a theme that I come back to in pretty much every one of my articles.

Plus, there’s all sorts of ridiculousness out there when it comes to improving mitochondrial function, including completely misguided recommendations like ketogenic diets and fasting, which often steer people astray. I’ll cover these topics in future articles as well.

 

In the meantime, you can check out the free health and energy balance mini-course, which you can sign up for below! In this mini-course, I outline several of the more important factors affecting energy production and usage, how they affect our health, and what you can do about them.

 

References

The Mythical Calorie Equation

Calories In – Calorie Out = Change in Body Fat

This ubiquitous equation represents the idea that the difference between the number of calories we consume and the number of calories we expend determines the amount of fat we gain or lose. It’s a wonderfully simple conception, although not an accurate one, and actually a very dangerous one.

It’s truly amazing to me that this equation has stuck around this long. The entire concept is illogical to begin with, not to mention the mounds of evidence against it.

Yet, the dogmatic adherence to this equation has informed so much of the current nutrition recommendations. This is especially true when it comes to fat loss, where “eat less and exercise more” is the common mantra. But it has also been applied to the general health recommendations to eat foods that are less calorie-dense, drink more water, and consume more protein and fiber to keep us full for longer, among many others.

While the fact that we associate calories with fat gain and loss is bad, the fact that we associate them with health is even worse.

But before we dive in too far, let’s start by exploring the extensive evidence that refutes the validity of equation.

Isocaloric Studies

If the calorie equation was valid, then consuming diets containing different foods with the same number of calories would have the same effects on body fat. But, many studies that have tested this hypothesis have shown that this isn’t the case. Let’s take a look at a few of them.

This first study, performed in a metabolic ward, had subjects on isocaloric reduced-fat or reduced-carbohydrate diets (1) (isocaloric means the diets had the same number of calories). They found that subjects on the reduced-fat diets lost more body fat than subjects on the reduced-carb diets. And, those on the reduced-fat diets lost less weight than those on the reduced-carb diets, meaning that a much higher percentage of the weight they lost was fat.

[This study also provides more evidence against the “burn fat for fat loss” fallacy, as those on the reduced-carb diets burned more fat than the reduced-fat group even though they lost less body fat.]

This next study also compared subjects on isocaloric diets with varying amounts of carbs and fat, although this one was performed on rats instead of humans (2). They found that the rats on the high-fat diets had higher total body fat by the end of the study than those on the control diet, but those on the high-carb diets didn’t. Again, remember that the high-fat and high-carb rats were fed the exact same number of calories!

In this study, human subjects were given 1 of 3 isocaloric diets that contained varying amounts of carbohydrates, and they found huge differences in weight loss, fat loss, and percent weight loss based on the amount of carbohydrates in the diet (3). In fact, those on the diet that was highest in carbohydrates lost 14 pounds more of body fat than those on the lowest carbohydrate diet during the 9-week intervention! In reference to these results, the authors commented that “no adequate explanation [could] be given for [the] weight loss differences.”

There are many more isocaloric studies that provide similar evidence against the calorie equation, including one on rats where two groups were fed the exact same diet except for the type of protein and ended up with a 26% difference in fat mass (4) and other studies showing that changing the amount of fat or carbohydrate in the diet affected the amount of body fat gained or lost, even when consuming the same number of calories (5, 6).

It’s clear based on these studies that the calorie equation isn’t quite as simple as it was made out to be. The types of foods that are eaten have a substantial effect on changes in body fat, rather than simply the number of “calories-in.”

Now, the argument can be made that changing the types of foods simply changes the number of “calories-out.” And, while this is true, it’s often entirely ignored in favor of the recommendations to simply “eat less and exercise more.”

Even when not ignored, the fact that the type of food, rather than simply the number of calories, affects the number of “calories-out” creates problems of its own.

It’s known that different diet compositions can vary in their metabolizable energy (the amount of energy in the food that’s actually digested and absorbed) and thermic effects (the amount of energy required for digesting and using the food). It’s also acknowledged that different diet compositions can cause changes in the resting metabolic rate and physical activity levels. But, some of the effects of different diet compositions can’t be fully explained yet.

This review, aimed at figuring out whether we can account for all the energetic effects of different diet compositions, looked at many calorie-controlled weight loss studies (7). They found that “neither macronutrient-specific differences in the availability of dietary energy nor changes in energy expenditure could explain [the] differences in weight loss” and concluded by suggesting that “further research is needed to identify the mechanisms that result in greater weight loss with one diet than with another.”

In other words, even if we account for differences in metabolizable energy, thermic effects, resting metabolic rate, and physical activity levels, (which very few people are doing) there are still unknown variables that would need to be factored in to make the calorie equation work.

This presents a glaring problem with this equation, but it doesn’t end here. There are other, more serious problems with the calorie equation that arise because it’s predicated on several false assumptions.

Caloric Restriction, Metabolic Adaptation, and Behavioral Compensation

The first of these assumptions is that our bodies’ energy usage doesn’t change based on our environment.

There have been many times where researchers have tried to apply the calorie equation to fat loss. They set up experiments where they reduce people’s food intakes and increase their exercise, thereby reducing the number of “calories-in” and increasing the number of “calories-out.”

And these studies do result in weight loss. But the amount of weight loss is nowhere near the amount predicted by the calorie equation.

This discrepancy boils down to two main factors:

1. Metabolic Adaptation

Metabolic adaptation is how our bodies internally adjust, or adapt, to changes in caloric intake (“calories-in”) or caloric expenditure (“calories-out”). When we reduce our caloric intake or increase our caloric expenditure, our bodies reduce the amount of energy they use. And when we increase our caloric intake or decrease our caloric expenditure, our bodies increase the amount of energy they use (8, 9, 10, 11).

This is accomplished through various hormonal and enzymatic changes, which allow for adjustments in energy usage, metabolic fuel selection, and energy partitioning.

These adaptive responses throw another wrench in the calorie equation. If we factor metabolic adaptation into the equation, we would have to reduce our caloric intake even more to achieve our desired weight loss.

2. Behavioral Compensation

Behavioral compensation is how we respond externally to changes in caloric intake or expenditure. This could mean reducing the amount we exercise when we eat fewer calories or increasing the amount we eat when we exercise more.

One review that considered many weight loss studies found that, because of behavioral compensation, the amount of weight loss from caloric restriction averages to be 12-44% less than what’s predicted by the calorie equation (12). They also found the amount of weight loss from increased exercise to be 55-64% less than was expected due to behavioral compensation.

Those are HUGE differences between the mythical calorie equation and reality!

And, behavioral compensation is an even bigger factor when we increase the amount of “calories-in.” The amount of weight gain in these situations is up to 96% less than is expected from the calorie equation! (12) You read that right, 96%! That basically means that we’re really good at compensating when we eat more food than normal, to the point that it’s pretty hard to gain weight that way.

But of course, metabolic adaptation and behavioral compensation don’t mean that the mythical equation is wrong. They’re just two more variables we have to factor into the equation that at this point is unrecognizable compared to the original “calories in – calories out = change in body fat.”

Up until this point we’ve only been dealing with adjustments to the calorie equation, but after considering this next false assumption it’ll become quite clear that this equation has no place in the health or fat loss arena.

What Are Calories?

This brings us to one of the most egregious errors that underlies the calorie equation: Calories are not relevant to human physiology.

Calories are simply a measure of energy, specifically heat energy.

In the context of nutrition, we think about the number of calories, or potential energy, held in certain foods. But, we can consider the number of calories in anything, whether it’s grass, wood, or gasoline.

Now, we all know that our bodies can’t convert the energy (calories) in grass, wood, or gasoline to usable energy in our bodies. So why do we assume that we’ll equally convert the energy in all food to usable energy in our bodies?

We consider that a mango has 200 calories, a steak has 600 calories, and a doughnut has 300 calories, but we don’t consider how much of that potential energy can or will be converted to usable energy.

There are many factors that affect how much of the energy, or calories, in the food we eat will become usable energy in our bodies.

The food must first be digested and absorbed. However, the amount of the food that actually gets digested and absorbed varies greatly based on the food and our gut function, and varying amounts of energy are required for this digestion and absorption.

Once absorbed, the carbohydrates, fats, and protein from the food we eat can be used to produce energy. This occurs in the mitochondria of our cells through a process called respiration.

During this process, the food we eat is converted into a form of usable energy that’s held in a molecule called ATP. But, there are tons of factors that affect whether the carbohydrates, fats, and protein even get to the mitochondria, let alone whether they’ll be used to produce ATP.

The different macronutrients (carbs, fats, and protein) vary significantly in this regard. Carbohydrates are our primary energy source while fat is our secondary energy source. Protein, on the other hand, is not likely to be converted to usable energy through mitochondrial respiration and is instead used primarily for building and rebuilding tissues.

So, it makes little sense to equate the potential energy, or calories, between the different macronutrients, as the likelihood that they’ll be used to produce ATP varies considerably. Equating the calories between the different macronutrients actually violates the second law of thermodynamics, as is explained here:

“A review of simple thermodynamic principles shows that weight change on isocaloric diets is not expected to be independent of path (metabolism of macronutrients) and indeed such a general principle would be a violation of the second law [of thermodynamics].” “The second law of thermodynamics says that variation of efficiency for different metabolic pathways is to be expected. Thus, ironically the dictum that a “calorie is a calorie” violates the second law of thermodynamics, as a matter of principle.” (13)

And, the factors that affect mitochondrial respiration go far beyond the differences between macronutrients. They also include the hormonal state, the amount of nutrients available, the toxins present, the time of day, the ambient temperature, the amount of sunlight present, the psychological state, and virtually every other aspect of our environment.

In other words, our bodies don’t run on a calorie currency, as they must convert the energy in food that we call “calories” into energy that they can use. And the amount of calories in our food is barely relevant considering the many factors that affect its conversion to usable energy.

The problems with the misplaced focus on calories has been nicely summed up in this quote:

“It is increasingly clear that the idea that “a calorie is a calorie” is misleading… Different diets… lead to different biochemical pathways (due to the hormonal and enzymatic changes) that are not equivalent when correctly compared through the laws of thermodynamics. Unless one measures heat and the biomolecules synthesized using ATP, it is inappropriate to assume that the only thing that counts in terms of food consumption and energy balance is the intake of dietary calories and weight storage.” (6)

And, as if all of this weren’t enough, the amount of usable energy that we do produce or use doesn’t say anything about where or what that energy is used for, which is vitally important to consider for both fat loss and health!

The Dangers of Caloric Restriction

The final false assumption of the calorie equation is that any excess energy we have will become fat, while any energy deficit will result in fat loss.

This assumption that fat gain is the product of excess energy and fat loss is the product of a lack of energy is probably the single most harmful misconception that exists in the health and nutrition field.

The 1st law of thermodynamics is often cited in support of this idea, which explains that energy cannot be created or destroyed. But, this has nothing to do with where energy is used or the physiological processes of fat gain and loss.

Energy is used for virtually everything we do. It’s used to accomplish our basic daily functions, like breathing and digesting, in addition to handling stressors, like exercise and mental work. Energy is also used to maintain, repair, and grow our tissues, like muscles, bones, fascia, and organs.

All the factors we’ve mentioned so far, including our hormonal state and the many aspects of our environment, determine the partitioning of energy, or where energy is used.

For example, in the rat study that was mentioned earlier, the amount of energy from consumed protein that was allocated to fat and muscle tissue differed based on the type of protein that was consumed (4).

However, the calorie equation doesn’t acknowledge the concept of energy partitioning and instead relies on the extremely common fallacy that any excess energy we have will be used for body fat and any energy deficit will come from body fat.

While this ignores a key physiological concept, there’s another problem with this fallacy that we haven’t addressed: body fat is a storage of fuel, or potential energy. In other words, the potential energy in food is stored as body fat when it’s NOT converted to usable energy.

While this is somewhat acknowledged, it’s assumed that energy production occurs until we have enough energy, at which point any potential energy left over becomes fat. But, that couldn’t be farther from the truth.

As was mentioned earlier, energy production, or mitochondrial respiration, is affected by all sorts of variables, from the amount of nutrients available to the time of day. When energy production is inhibited based on these many factors, the potential energy from our food is stored as fat and we’re left without enough energy to properly function.

This is what underlies fat gain and the obesity epidemic. Not too much energy, but too little energy (14).

As such, the recommendations to further reduce our available energy only make the problem worse, as is explained in this quote:

“In conclusion, the presented metabolic mechanism of environmentally caused obesity indicates energy deficiency as an engine working toward development of obesity. It is obvious that all efforts to stop this engine by further decreasing the energy cannot be successful. Thus, the low calorie diets and exercise regimens seem to be a redundant burden of already exhausted people.” (14)

Unfortunately, it doesn’t end there. Our bodies adapt to energy deficiencies by further inhibiting energy production and storing more fuel as fat in order to conserve energy, resulting in a vicious cycle (10, 14, 15).

This is the biggest reason why the calorie equation is destroying our health. We already lack energy due to the inhibition of mitochondrial respiration by nutrient deficiencies and many other problems, and then we eat less and exercise more, which further reduces the amount of energy we have available to properly function, encourages fat gain, and leads to the chronic diseases we see in epidemic proportions today.

We need to put an end to this terribly misguided approach to fat loss and health and instead shift our focus to the process of energy production. By increasing the amount of energy we produce, we can reduce the storage of food as body fat which will allow us to lose fat while also improving our health.

As I’m sure you’ve already gathered, there are quite a few factors affecting energy production. If you want to learn more about those factors and learn to lose fat the healthy way, sign up for the free mini-course below!

References

The Mythical Calorie Equation

Calories In – Calorie Out = Change in Body Fat

This ubiquitous equation represents the idea that the difference between the number of calories we consume and the number of calories we expend determines the amount of fat we gain or lose. It’s a wonderfully simple conception, although not an accurate one, and actually a very dangerous one.

It’s truly amazing to me that this equation has stuck around this long. The entire concept is illogical to begin with, not to mention the mounds of evidence against it.

Yet, the dogmatic adherence to this equation has informed so much of the current nutrition recommendations. This is especially true when it comes to fat loss, where “eat less and exercise more” is the common mantra. But it has also been applied to the general health recommendations to eat foods that are less calorie-dense, drink more water, and consume more protein and fiber to keep us full for longer, among many others.

While the fact that we associate calories with fat gain and loss is bad, the fact that we associate them with health is even worse.

But before we dive in too far, let’s start by exploring the extensive evidence that refutes the validity of equation.

Isocaloric Studies

If the calorie equation was valid, then consuming diets containing different foods with the same number of calories would have the same effects on body fat. But, many studies that have tested this hypothesis have shown that this isn’t the case. Let’s take a look at a few of them.

This first study, performed in a metabolic ward, had subjects on isocaloric reduced-fat or reduced-carbohydrate diets (1) (isocaloric means the diets had the same number of calories). They found that subjects on the reduced-fat diets lost more body fat than subjects on the reduced-carb diets. And, those on the reduced-fat diets lost less weight than those on the reduced-carb diets, meaning that a much higher percentage of the weight they lost was fat.

[This study also provides more evidence against the “burn fat for fat loss” fallacy, as those on the reduced-carb diets burned more fat than the reduced-fat group even though they lost less body fat.]

This next study also compared subjects on isocaloric diets with varying amounts of carbs and fat, although this one was performed on rats instead of humans (2). They found that the rats on the high-fat diets had higher total body fat by the end of the study than those on the control diet, but those on the high-carb diets didn’t. Again, remember that the high-fat and high-carb rats were fed the exact same number of calories!

In this study, human subjects were given 1 of 3 isocaloric diets that contained varying amounts of carbohydrates, and they found huge differences in weight loss, fat loss, and percent weight loss based on the amount of carbohydrates in the diet (3). In fact, those on the diet that was highest in carbohydrates lost 14 pounds more of body fat than those on the lowest carbohydrate diet during the 9-week intervention! In reference to these results, the authors commented that “no adequate explanation [could] be given for [the] weight loss differences.”

There are many more isocaloric studies that provide similar evidence against the calorie equation, including one on rats where two groups were fed the exact same diet except for the type of protein and ended up with a 26% difference in fat mass (4) and other studies showing that changing the amount of fat or carbohydrate in the diet affected the amount of body fat gained or lost, even when consuming the same number of calories (5, 6).

It’s clear based on these studies that the calorie equation isn’t quite as simple as it was made out to be. The types of foods that are eaten have a substantial effect on changes in body fat, rather than simply the number of “calories-in.”

Now, the argument can be made that changing the types of foods simply changes the number of “calories-out.” And, while this is true, it’s often entirely ignored in favor of the recommendations to simply “eat less and exercise more.”

Even when not ignored, the fact that the type of food, rather than simply the number of calories, affects the number of “calories-out” creates problems of its own.

It’s known that different diet compositions can vary in their metabolizable energy (the amount of energy in the food that’s actually digested and absorbed) and thermic effects (the amount of energy required for digesting and using the food). It’s also acknowledged that different diet compositions can cause changes in the resting metabolic rate and physical activity levels. But, some of the effects of different diet compositions can’t be fully explained yet.

This review, aimed at figuring out whether we can account for all the energetic effects of different diet compositions, looked at many calorie-controlled weight loss studies (7). They found that “neither macronutrient-specific differences in the availability of dietary energy nor changes in energy expenditure could explain [the] differences in weight loss” and concluded by suggesting that “further research is needed to identify the mechanisms that result in greater weight loss with one diet than with another.”

In other words, even if we account for differences in metabolizable energy, thermic effects, resting metabolic rate, and physical activity levels, (which very few people are doing) there are still unknown variables that would need to be factored in to make the calorie equation work.

This presents a glaring problem with this equation, but it doesn’t end here. There are other, more serious problems with the calorie equation that arise because it’s predicated on several false assumptions.

Caloric Restriction, Metabolic Adaptation, and Behavioral Compensation

The first of these assumptions is that our bodies’ energy usage doesn’t change based on our environment.

There have been many times where researchers have tried to apply the calorie equation to fat loss. They set up experiments where they reduce people’s food intakes and increase their exercise, thereby reducing the number of “calories-in” and increasing the number of “calories-out.”

And these studies do result in weight loss. But the amount of weight loss is nowhere near the amount predicted by the calorie equation.

This discrepancy boils down to two main factors:

1. Metabolic Adaptation

Metabolic adaptation is how our bodies internally adjust, or adapt, to changes in caloric intake (“calories-in”) or caloric expenditure (“calories-out”). When we reduce our caloric intake or increase our caloric expenditure, our bodies reduce the amount of energy they use. And when we increase our caloric intake or decrease our caloric expenditure, our bodies increase the amount of energy they use (8, 9, 10, 11).

This is accomplished through various hormonal and enzymatic changes, which allow for adjustments in energy usage, metabolic fuel selection, and energy partitioning.

These adaptive responses throw another wrench in the calorie equation. If we factor metabolic adaptation into the equation, we would have to reduce our caloric intake even more to achieve our desired weight loss.

2. Behavioral Compensation

Behavioral compensation is how we respond externally to changes in caloric intake or expenditure. This could mean reducing the amount we exercise when we eat fewer calories or increasing the amount we eat when we exercise more.

One review that considered many weight loss studies found that, because of behavioral compensation, the amount of weight loss from caloric restriction averages to be 12-44% less than what’s predicted by the calorie equation (12). They also found the amount of weight loss from increased exercise to be 55-64% less than was expected due to behavioral compensation.

Those are HUGE differences between the mythical calorie equation and reality!

And, behavioral compensation is an even bigger factor when we increase the amount of “calories-in.” The amount of weight gain in these situations is up to 96% less than is expected from the calorie equation! (12) You read that right, 96%! That basically means that we’re really good at compensating when we eat more food than normal, to the point that it’s pretty hard to gain weight that way.

But of course, metabolic adaptation and behavioral compensation don’t mean that the mythical equation is wrong. They’re just two more variables we have to factor into the equation that at this point is unrecognizable compared to the original “calories in – calories out = change in body fat.”

Up until this point we’ve only been dealing with adjustments to the calorie equation, but after considering this next false assumption it’ll become quite clear that this equation has no place in the health or fat loss arena.

What Are Calories?

This brings us to one of the most egregious errors that underlies the calorie equation: Calories are not relevant to human physiology.

Calories are simply a measure of energy, specifically heat energy.

In the context of nutrition, we think about the number of calories, or potential energy, held in certain foods. But, we can consider the number of calories in anything, whether it’s grass, wood, or gasoline.

Now, we all know that our bodies can’t convert the energy (calories) in grass, wood, or gasoline to usable energy in our bodies. So why do we assume that we’ll equally convert the energy in all food to usable energy in our bodies?

We consider that a mango has 200 calories, a steak has 600 calories, and a doughnut has 300 calories, but we don’t consider how much of that potential energy can or will be converted to usable energy.

There are many factors that affect how much of the energy, or calories, in the food we eat will become usable energy in our bodies.

The food must first be digested and absorbed. However, the amount of the food that actually gets digested and absorbed varies greatly based on the food and our gut function, and varying amounts of energy are required for this digestion and absorption.

Once absorbed, the carbohydrates, fats, and protein from the food we eat can be used to produce energy. This occurs in the mitochondria of our cells through a process called respiration.

During this process, the food we eat is converted into a form of usable energy that’s held in a molecule called ATP. But, there are tons of factors that affect whether the carbohydrates, fats, and protein even get to the mitochondria, let alone whether they’ll be used to produce ATP.

The different macronutrients (carbs, fats, and protein) vary significantly in this regard. Carbohydrates are our primary energy source while fat is our secondary energy source. Protein, on the other hand, is not likely to be converted to usable energy through mitochondrial respiration and is instead used primarily for building and rebuilding tissues.

So, it makes little sense to equate the potential energy, or calories, between the different macronutrients, as the likelihood that they’ll be used to produce ATP varies considerably. Equating the calories between the different macronutrients actually violates the second law of thermodynamics, as is explained here:

“A review of simple thermodynamic principles shows that weight change on isocaloric diets is not expected to be independent of path (metabolism of macronutrients) and indeed such a general principle would be a violation of the second law [of thermodynamics].” “The second law of thermodynamics says that variation of efficiency for different metabolic pathways is to be expected. Thus, ironically the dictum that a “calorie is a calorie” violates the second law of thermodynamics, as a matter of principle.” (13)

And, the factors that affect mitochondrial respiration go far beyond the differences between macronutrients. They also include the hormonal state, the amount of nutrients available, the toxins present, the time of day, the ambient temperature, the amount of sunlight present, the psychological state, and virtually every other aspect of our environment.

In other words, our bodies don’t run on a calorie currency, as they must convert the energy in food that we call “calories” into energy that they can use. And the amount of calories in our food is barely relevant considering the many factors that affect its conversion to usable energy.

The problems with the misplaced focus on calories has been nicely summed up in this quote:

“It is increasingly clear that the idea that “a calorie is a calorie” is misleading… Different diets… lead to different biochemical pathways (due to the hormonal and enzymatic changes) that are not equivalent when correctly compared through the laws of thermodynamics. Unless one measures heat and the biomolecules synthesized using ATP, it is inappropriate to assume that the only thing that counts in terms of food consumption and energy balance is the intake of dietary calories and weight storage.” (6)

And, as if all of this weren’t enough, the amount of usable energy that we do produce or use doesn’t say anything about where or what that energy is used for, which is vitally important to consider for both fat loss and health!

The Dangers of Caloric Restriction

The final false assumption of the calorie equation is that any excess energy we have will become fat, while any energy deficit will result in fat loss.

This assumption that fat gain is the product of excess energy and fat loss is the product of a lack of energy is probably the single most harmful misconception that exists in the health and nutrition field.

The 1st law of thermodynamics is often cited in support of this idea, which explains that energy cannot be created or destroyed. But, this has nothing to do with where energy is used or the physiological processes of fat gain and loss.

Energy is used for virtually everything we do. It’s used to accomplish our basic daily functions, like breathing and digesting, in addition to handling stressors, like exercise and mental work. Energy is also used to maintain, repair, and grow our tissues, like muscles, bones, fascia, and organs.

All the factors we’ve mentioned so far, including our hormonal state and the many aspects of our environment, determine the partitioning of energy, or where energy is used.

For example, in the rat study that was mentioned earlier, the amount of energy from consumed protein that was allocated to fat and muscle tissue differed based on the type of protein that was consumed (4).

However, the calorie equation doesn’t acknowledge the concept of energy partitioning and instead relies on the extremely common fallacy that any excess energy we have will be used for body fat and any energy deficit will come from body fat.

While this ignores a key physiological concept, there’s another problem with this fallacy that we haven’t addressed: body fat is a storage of fuel, or potential energy. In other words, the potential energy in food is stored as body fat when it’s NOT converted to usable energy.

While this is somewhat acknowledged, it’s assumed that energy production occurs until we have enough energy, at which point any potential energy left over becomes fat. But, that couldn’t be farther from the truth.

As was mentioned earlier, energy production, or mitochondrial respiration, is affected by all sorts of variables, from the amount of nutrients available to the time of day. When energy production is inhibited based on these many factors, the potential energy from our food is stored as fat and we’re left without enough energy to properly function.

This is what underlies fat gain and the obesity epidemic. Not too much energy, but too little energy (14).

As such, the recommendations to further reduce our available energy only make the problem worse, as is explained in this quote:

“In conclusion, the presented metabolic mechanism of environmentally caused obesity indicates energy deficiency as an engine working toward development of obesity. It is obvious that all efforts to stop this engine by further decreasing the energy cannot be successful. Thus, the low calorie diets and exercise regimens seem to be a redundant burden of already exhausted people.” (14)

Unfortunately, it doesn’t end there. Our bodies adapt to energy deficiencies by further inhibiting energy production and storing more fuel as fat in order to conserve energy, resulting in a vicious cycle (10, 14, 15).

This is the biggest reason why the calorie equation is destroying our health. We already lack energy due to the inhibition of mitochondrial respiration by nutrient deficiencies and many other problems, and then we eat less and exercise more, which further reduces the amount of energy we have available to properly function, encourages fat gain, and leads to the chronic diseases we see in epidemic proportions today.

We need to put an end to this terribly misguided approach to fat loss and health and instead shift our focus to the process of energy production. By increasing the amount of energy we produce, we can reduce the storage of food as body fat which will allow us to lose fat while also improving our health.

As I’m sure you’ve already gathered, there are quite a few factors affecting energy production. If you want to learn more about those factors and learn to lose fat the healthy way, sign up for the free mini-course below!

References

The Mythical Calorie Equation

Calories In – Calorie Out = Change in Body Fat

This ubiquitous equation represents the idea that the difference between the number of calories we consume and the number of calories we expend determines the amount of fat we gain or lose. It’s a wonderfully simple conception, although not an accurate one, and actually a very dangerous one.

It’s truly amazing to me that this equation has stuck around this long. The entire concept is illogical to begin with, not to mention the mounds of evidence against it.

Yet, the dogmatic adherence to this equation has informed so much of the current nutrition recommendations. This is especially true when it comes to fat loss, where “eat less and exercise more” is the common mantra. But it has also been applied to the general health recommendations to eat foods that are less calorie-dense, drink more water, and consume more protein and fiber to keep us full for longer, among many others.

While the fact that we associate calories with fat gain and loss is bad, the fact that we associate them with health is even worse.

But before we dive in too far, let’s start by exploring the extensive evidence that refutes the validity of equation.

Isocaloric Studies

If the calorie equation was valid, then consuming diets containing different foods with the same number of calories would have the same effects on body fat. But, many studies that have tested this hypothesis have shown that this isn’t the case. Let’s take a look at a few of them.

This first study, performed in a metabolic ward, had subjects on isocaloric reduced-fat or reduced-carbohydrate diets (1) (isocaloric means the diets had the same number of calories). They found that subjects on the reduced-fat diets lost more body fat than subjects on the reduced-carb diets. And, those on the reduced-fat diets lost less weight than those on the reduced-carb diets, meaning that a much higher percentage of the weight they lost was fat.

[This study also provides more evidence against the “burn fat for fat loss” fallacy, as those on the reduced-carb diets burned more fat than the reduced-fat group even though they lost less body fat.]

This next study also compared subjects on isocaloric diets with varying amounts of carbs and fat, although this one was performed on rats instead of humans (2). They found that the rats on the high-fat diets had higher total body fat by the end of the study than those on the control diet, but those on the high-carb diets didn’t. Again, remember that the high-fat and high-carb rats were fed the exact same number of calories!

In this study, human subjects were given 1 of 3 isocaloric diets that contained varying amounts of carbohydrates, and they found huge differences in weight loss, fat loss, and percent weight loss based on the amount of carbohydrates in the diet (3). In fact, those on the diet that was highest in carbohydrates lost 14 pounds more of body fat than those on the lowest carbohydrate diet during the 9-week intervention! In reference to these results, the authors commented that “no adequate explanation [could] be given for [the] weight loss differences.”

There are many more isocaloric studies that provide similar evidence against the calorie equation, including one on rats where two groups were fed the exact same diet except for the type of protein and ended up with a 26% difference in fat mass (4) and other studies showing that changing the amount of fat or carbohydrate in the diet affected the amount of body fat gained or lost, even when consuming the same number of calories (5, 6).

It’s clear based on these studies that the calorie equation isn’t quite as simple as it was made out to be. The types of foods that are eaten have a substantial effect on changes in body fat, rather than simply the number of “calories-in.”

Now, the argument can be made that changing the types of foods simply changes the number of “calories-out.” And, while this is true, it’s often entirely ignored in favor of the recommendations to simply “eat less and exercise more.”

Even when not ignored, the fact that the type of food, rather than simply the number of calories, affects the number of “calories-out” creates problems of its own.

It’s known that different diet compositions can vary in their metabolizable energy (the amount of energy in the food that’s actually digested and absorbed) and thermic effects (the amount of energy required for digesting and using the food). It’s also acknowledged that different diet compositions can cause changes in the resting metabolic rate and physical activity levels. But, some of the effects of different diet compositions can’t be fully explained yet.

This review, aimed at figuring out whether we can account for all the energetic effects of different diet compositions, looked at many calorie-controlled weight loss studies (7). They found that “neither macronutrient-specific differences in the availability of dietary energy nor changes in energy expenditure could explain [the] differences in weight loss” and concluded by suggesting that “further research is needed to identify the mechanisms that result in greater weight loss with one diet than with another.”

In other words, even if we account for differences in metabolizable energy, thermic effects, resting metabolic rate, and physical activity levels, (which very few people are doing) there are still unknown variables that would need to be factored in to make the calorie equation work.

This presents a glaring problem with this equation, but it doesn’t end here. There are other, more serious problems with the calorie equation that arise because it’s predicated on several false assumptions.

Caloric Restriction, Metabolic Adaptation, and Behavioral Compensation

The first of these assumptions is that our bodies’ energy usage doesn’t change based on our environment.

There have been many times where researchers have tried to apply the calorie equation to fat loss. They set up experiments where they reduce people’s food intakes and increase their exercise, thereby reducing the number of “calories-in” and increasing the number of “calories-out.”

And these studies do result in weight loss. But the amount of weight loss is nowhere near the amount predicted by the calorie equation.

This discrepancy boils down to two main factors:

1. Metabolic Adaptation

Metabolic adaptation is how our bodies internally adjust, or adapt, to changes in caloric intake (“calories-in”) or caloric expenditure (“calories-out”). When we reduce our caloric intake or increase our caloric expenditure, our bodies reduce the amount of energy they use. And when we increase our caloric intake or decrease our caloric expenditure, our bodies increase the amount of energy they use (8, 9, 10, 11).

This is accomplished through various hormonal and enzymatic changes, which allow for adjustments in energy usage, metabolic fuel selection, and energy partitioning.

These adaptive responses throw another wrench in the calorie equation. If we factor metabolic adaptation into the equation, we would have to reduce our caloric intake even more to achieve our desired weight loss.

2. Behavioral Compensation

Behavioral compensation is how we respond externally to changes in caloric intake or expenditure. This could mean reducing the amount we exercise when we eat fewer calories or increasing the amount we eat when we exercise more.

One review that considered many weight loss studies found that, because of behavioral compensation, the amount of weight loss from caloric restriction averages to be 12-44% less than what’s predicted by the calorie equation (12). They also found the amount of weight loss from increased exercise to be 55-64% less than was expected due to behavioral compensation.

Those are HUGE differences between the mythical calorie equation and reality!

And, behavioral compensation is an even bigger factor when we increase the amount of “calories-in.” The amount of weight gain in these situations is up to 96% less than is expected from the calorie equation! (12) You read that right, 96%! That basically means that we’re really good at compensating when we eat more food than normal, to the point that it’s pretty hard to gain weight that way.

But of course, metabolic adaptation and behavioral compensation don’t mean that the mythical equation is wrong. They’re just two more variables we have to factor into the equation that at this point is unrecognizable compared to the original “calories in – calories out = change in body fat.”

Up until this point we’ve only been dealing with adjustments to the calorie equation, but after considering this next false assumption it’ll become quite clear that this equation has no place in the health or fat loss arena.

What Are Calories?

This brings us to one of the most egregious errors that underlies the calorie equation: Calories are not relevant to human physiology.

Calories are simply a measure of energy, specifically heat energy.

In the context of nutrition, we think about the number of calories, or potential energy, held in certain foods. But, we can consider the number of calories in anything, whether it’s grass, wood, or gasoline.

Now, we all know that our bodies can’t convert the energy (calories) in grass, wood, or gasoline to usable energy in our bodies. So why do we assume that we’ll equally convert the energy in all food to usable energy in our bodies?

We consider that a mango has 200 calories, a steak has 600 calories, and a doughnut has 300 calories, but we don’t consider how much of that potential energy can or will be converted to usable energy.

There are many factors that affect how much of the energy, or calories, in the food we eat will become usable energy in our bodies.

The food must first be digested and absorbed. However, the amount of the food that actually gets digested and absorbed varies greatly based on the food and our gut function, and varying amounts of energy are required for this digestion and absorption.

Once absorbed, the carbohydrates, fats, and protein from the food we eat can be used to produce energy. This occurs in the mitochondria of our cells through a process called respiration.

During this process, the food we eat is converted into a form of usable energy that’s held in a molecule called ATP. But, there are tons of factors that affect whether the carbohydrates, fats, and protein even get to the mitochondria, let alone whether they’ll be used to produce ATP.

The different macronutrients (carbs, fats, and protein) vary significantly in this regard. Carbohydrates are our primary energy source while fat is our secondary energy source. Protein, on the other hand, is not likely to be converted to usable energy through mitochondrial respiration and is instead used primarily for building and rebuilding tissues.

So, it makes little sense to equate the potential energy, or calories, between the different macronutrients, as the likelihood that they’ll be used to produce ATP varies considerably. Equating the calories between the different macronutrients actually violates the second law of thermodynamics, as is explained here:

“A review of simple thermodynamic principles shows that weight change on isocaloric diets is not expected to be independent of path (metabolism of macronutrients) and indeed such a general principle would be a violation of the second law [of thermodynamics].” “The second law of thermodynamics says that variation of efficiency for different metabolic pathways is to be expected. Thus, ironically the dictum that a “calorie is a calorie” violates the second law of thermodynamics, as a matter of principle.” (13)

And, the factors that affect mitochondrial respiration go far beyond the differences between macronutrients. They also include the hormonal state, the amount of nutrients available, the toxins present, the time of day, the ambient temperature, the amount of sunlight present, the psychological state, and virtually every other aspect of our environment.

In other words, our bodies don’t run on a calorie currency, as they must convert the energy in food that we call “calories” into energy that they can use. And the amount of calories in our food is barely relevant considering the many factors that affect its conversion to usable energy.

The problems with the misplaced focus on calories has been nicely summed up in this quote:

“It is increasingly clear that the idea that “a calorie is a calorie” is misleading… Different diets… lead to different biochemical pathways (due to the hormonal and enzymatic changes) that are not equivalent when correctly compared through the laws of thermodynamics. Unless one measures heat and the biomolecules synthesized using ATP, it is inappropriate to assume that the only thing that counts in terms of food consumption and energy balance is the intake of dietary calories and weight storage.” (6)

And, as if all of this weren’t enough, the amount of usable energy that we do produce or use doesn’t say anything about where or what that energy is used for, which is vitally important to consider for both fat loss and health!

The Dangers of Caloric Restriction

The final false assumption of the calorie equation is that any excess energy we have will become fat, while any energy deficit will result in fat loss.

This assumption that fat gain is the product of excess energy and fat loss is the product of a lack of energy is probably the single most harmful misconception that exists in the health and nutrition field.

The 1st law of thermodynamics is often cited in support of this idea, which explains that energy cannot be created or destroyed. But, this has nothing to do with where energy is used or the physiological processes of fat gain and loss.

Energy is used for virtually everything we do. It’s used to accomplish our basic daily functions, like breathing and digesting, in addition to handling stressors, like exercise and mental work. Energy is also used to maintain, repair, and grow our tissues, like muscles, bones, fascia, and organs.

All the factors we’ve mentioned so far, including our hormonal state and the many aspects of our environment, determine the partitioning of energy, or where energy is used.

For example, in the rat study that was mentioned earlier, the amount of energy from consumed protein that was allocated to fat and muscle tissue differed based on the type of protein that was consumed (4).

However, the calorie equation doesn’t acknowledge the concept of energy partitioning and instead relies on the extremely common fallacy that any excess energy we have will be used for body fat and any energy deficit will come from body fat.

While this ignores a key physiological concept, there’s another problem with this fallacy that we haven’t addressed: body fat is a storage of fuel, or potential energy. In other words, the potential energy in food is stored as body fat when it’s NOT converted to usable energy.

While this is somewhat acknowledged, it’s assumed that energy production occurs until we have enough energy, at which point any potential energy left over becomes fat. But, that couldn’t be farther from the truth.

As was mentioned earlier, energy production, or mitochondrial respiration, is affected by all sorts of variables, from the amount of nutrients available to the time of day. When energy production is inhibited based on these many factors, the potential energy from our food is stored as fat and we’re left without enough energy to properly function.

This is what underlies fat gain and the obesity epidemic. Not too much energy, but too little energy (14).

As such, the recommendations to further reduce our available energy only make the problem worse, as is explained in this quote:

“In conclusion, the presented metabolic mechanism of environmentally caused obesity indicates energy deficiency as an engine working toward development of obesity. It is obvious that all efforts to stop this engine by further decreasing the energy cannot be successful. Thus, the low calorie diets and exercise regimens seem to be a redundant burden of already exhausted people.” (14)

Unfortunately, it doesn’t end there. Our bodies adapt to energy deficiencies by further inhibiting energy production and storing more fuel as fat in order to conserve energy, resulting in a vicious cycle (10, 14, 15).

This is the biggest reason why the calorie equation is destroying our health. We already lack energy due to the inhibition of mitochondrial respiration by nutrient deficiencies and many other problems, and then we eat less and exercise more, which further reduces the amount of energy we have available to properly function, encourages fat gain, and leads to the chronic diseases we see in epidemic proportions today.

We need to put an end to this terribly misguided approach to fat loss and health and instead shift our focus to the process of energy production. By increasing the amount of energy we produce, we can reduce the storage of food as body fat which will allow us to lose fat while also improving our health.

As I’m sure you’ve already gathered, there are quite a few factors affecting energy production. If you want to learn more about those factors and learn to lose fat the healthy way, sign up for the free mini-course below!

References

The Mythical Calorie Equation

Calories In – Calorie Out = Change in Body Fat

This ubiquitous equation represents the idea that the difference between the number of calories we consume and the number of calories we expend determines the amount of fat we gain or lose. It’s a wonderfully simple conception, although not an accurate one, and actually a very dangerous one.

It’s truly amazing to me that this equation has stuck around this long. The entire concept is illogical to begin with, not to mention the mounds of evidence against it.

Yet, the dogmatic adherence to this equation has informed so much of the current nutrition recommendations. This is especially true when it comes to fat loss, where “eat less and exercise more” is the common mantra. But it has also been applied to the general health recommendations to eat foods that are less calorie-dense, drink more water, and consume more protein and fiber to keep us full for longer, among many others.

While the fact that we associate calories with fat gain and loss is bad, the fact that we associate them with health is even worse.

But before we dive in too far, let’s start by exploring the extensive evidence that refutes the validity of equation.

Isocaloric Studies

If the calorie equation was valid, then consuming diets containing different foods with the same number of calories would have the same effects on body fat. But, many studies that have tested this hypothesis have shown that this isn’t the case. Let’s take a look at a few of them.

This first study, performed in a metabolic ward, had subjects on isocaloric reduced-fat or reduced-carbohydrate diets (1) (isocaloric means the diets had the same number of calories). They found that subjects on the reduced-fat diets lost more body fat than subjects on the reduced-carb diets. And, those on the reduced-fat diets lost less weight than those on the reduced-carb diets, meaning that a much higher percentage of the weight they lost was fat.

[This study also provides more evidence against the “burn fat for fat loss” fallacy, as those on the reduced-carb diets burned more fat than the reduced-fat group even though they lost less body fat.]

This next study also compared subjects on isocaloric diets with varying amounts of carbs and fat, although this one was performed on rats instead of humans (2). They found that the rats on the high-fat diets had higher total body fat by the end of the study than those on the control diet, but those on the high-carb diets didn’t. Again, remember that the high-fat and high-carb rats were fed the exact same number of calories!

In this study, human subjects were given 1 of 3 isocaloric diets that contained varying amounts of carbohydrates, and they found huge differences in weight loss, fat loss, and percent weight loss based on the amount of carbohydrates in the diet (3). In fact, those on the diet that was highest in carbohydrates lost 14 pounds more of body fat than those on the lowest carbohydrate diet during the 9-week intervention! In reference to these results, the authors commented that “no adequate explanation [could] be given for [the] weight loss differences.”

There are many more isocaloric studies that provide similar evidence against the calorie equation, including one on rats where two groups were fed the exact same diet except for the type of protein and ended up with a 26% difference in fat mass (4) and other studies showing that changing the amount of fat or carbohydrate in the diet affected the amount of body fat gained or lost, even when consuming the same number of calories (5, 6).

It’s clear based on these studies that the calorie equation isn’t quite as simple as it was made out to be. The types of foods that are eaten have a substantial effect on changes in body fat, rather than simply the number of “calories-in.”

Now, the argument can be made that changing the types of foods simply changes the number of “calories-out.” And, while this is true, it’s often entirely ignored in favor of the recommendations to simply “eat less and exercise more.”

Even when not ignored, the fact that the type of food, rather than simply the number of calories, affects the number of “calories-out” creates problems of its own.

It’s known that different diet compositions can vary in their metabolizable energy (the amount of energy in the food that’s actually digested and absorbed) and thermic effects (the amount of energy required for digesting and using the food). It’s also acknowledged that different diet compositions can cause changes in the resting metabolic rate and physical activity levels. But, some of the effects of different diet compositions can’t be fully explained yet.

This review, aimed at figuring out whether we can account for all the energetic effects of different diet compositions, looked at many calorie-controlled weight loss studies (7). They found that “neither macronutrient-specific differences in the availability of dietary energy nor changes in energy expenditure could explain [the] differences in weight loss” and concluded by suggesting that “further research is needed to identify the mechanisms that result in greater weight loss with one diet than with another.”

In other words, even if we account for differences in metabolizable energy, thermic effects, resting metabolic rate, and physical activity levels, (which very few people are doing) there are still unknown variables that would need to be factored in to make the calorie equation work.

This presents a glaring problem with this equation, but it doesn’t end here. There are other, more serious problems with the calorie equation that arise because it’s predicated on several false assumptions.

Caloric Restriction, Metabolic Adaptation, and Behavioral Compensation

The first of these assumptions is that our bodies’ energy usage doesn’t change based on our environment.

There have been many times where researchers have tried to apply the calorie equation to fat loss. They set up experiments where they reduce people’s food intakes and increase their exercise, thereby reducing the number of “calories-in” and increasing the number of “calories-out.”

And these studies do result in weight loss. But the amount of weight loss is nowhere near the amount predicted by the calorie equation.

This discrepancy boils down to two main factors:

1. Metabolic Adaptation

Metabolic adaptation is how our bodies internally adjust, or adapt, to changes in caloric intake (“calories-in”) or caloric expenditure (“calories-out”). When we reduce our caloric intake or increase our caloric expenditure, our bodies reduce the amount of energy they use. And when we increase our caloric intake or decrease our caloric expenditure, our bodies increase the amount of energy they use (8, 9, 10, 11).

This is accomplished through various hormonal and enzymatic changes, which allow for adjustments in energy usage, metabolic fuel selection, and energy partitioning.

These adaptive responses throw another wrench in the calorie equation. If we factor metabolic adaptation into the equation, we would have to reduce our caloric intake even more to achieve our desired weight loss.

2. Behavioral Compensation

Behavioral compensation is how we respond externally to changes in caloric intake or expenditure. This could mean reducing the amount we exercise when we eat fewer calories or increasing the amount we eat when we exercise more.

One review that considered many weight loss studies found that, because of behavioral compensation, the amount of weight loss from caloric restriction averages to be 12-44% less than what’s predicted by the calorie equation (12). They also found the amount of weight loss from increased exercise to be 55-64% less than was expected due to behavioral compensation.

Those are HUGE differences between the mythical calorie equation and reality!

And, behavioral compensation is an even bigger factor when we increase the amount of “calories-in.” The amount of weight gain in these situations is up to 96% less than is expected from the calorie equation! (12) You read that right, 96%! That basically means that we’re really good at compensating when we eat more food than normal, to the point that it’s pretty hard to gain weight that way.

But of course, metabolic adaptation and behavioral compensation don’t mean that the mythical equation is wrong. They’re just two more variables we have to factor into the equation that at this point is unrecognizable compared to the original “calories in – calories out = change in body fat.”

Up until this point we’ve only been dealing with adjustments to the calorie equation, but after considering this next false assumption it’ll become quite clear that this equation has no place in the health or fat loss arena.

What Are Calories?

This brings us to one of the most egregious errors that underlies the calorie equation: Calories are not relevant to human physiology.

Calories are simply a measure of energy, specifically heat energy.

In the context of nutrition, we think about the number of calories, or potential energy, held in certain foods. But, we can consider the number of calories in anything, whether it’s grass, wood, or gasoline.

Now, we all know that our bodies can’t convert the energy (calories) in grass, wood, or gasoline to usable energy in our bodies. So why do we assume that we’ll equally convert the energy in all food to usable energy in our bodies?

We consider that a mango has 200 calories, a steak has 600 calories, and a doughnut has 300 calories, but we don’t consider how much of that potential energy can or will be converted to usable energy.

There are many factors that affect how much of the energy, or calories, in the food we eat will become usable energy in our bodies.

The food must first be digested and absorbed. However, the amount of the food that actually gets digested and absorbed varies greatly based on the food and our gut function, and varying amounts of energy are required for this digestion and absorption.

Once absorbed, the carbohydrates, fats, and protein from the food we eat can be used to produce energy. This occurs in the mitochondria of our cells through a process called respiration.

During this process, the food we eat is converted into a form of usable energy that’s held in a molecule called ATP. But, there are tons of factors that affect whether the carbohydrates, fats, and protein even get to the mitochondria, let alone whether they’ll be used to produce ATP.

The different macronutrients (carbs, fats, and protein) vary significantly in this regard. Carbohydrates are our primary energy source while fat is our secondary energy source. Protein, on the other hand, is not likely to be converted to usable energy through mitochondrial respiration and is instead used primarily for building and rebuilding tissues.

So, it makes little sense to equate the potential energy, or calories, between the different macronutrients, as the likelihood that they’ll be used to produce ATP varies considerably. Equating the calories between the different macronutrients actually violates the second law of thermodynamics, as is explained here:

“A review of simple thermodynamic principles shows that weight change on isocaloric diets is not expected to be independent of path (metabolism of macronutrients) and indeed such a general principle would be a violation of the second law [of thermodynamics].” “The second law of thermodynamics says that variation of efficiency for different metabolic pathways is to be expected. Thus, ironically the dictum that a “calorie is a calorie” violates the second law of thermodynamics, as a matter of principle.” (13)

And, the factors that affect mitochondrial respiration go far beyond the differences between macronutrients. They also include the hormonal state, the amount of nutrients available, the toxins present, the time of day, the ambient temperature, the amount of sunlight present, the psychological state, and virtually every other aspect of our environment.

In other words, our bodies don’t run on a calorie currency, as they must convert the energy in food that we call “calories” into energy that they can use. And the amount of calories in our food is barely relevant considering the many factors that affect its conversion to usable energy.

The problems with the misplaced focus on calories has been nicely summed up in this quote:

“It is increasingly clear that the idea that “a calorie is a calorie” is misleading… Different diets… lead to different biochemical pathways (due to the hormonal and enzymatic changes) that are not equivalent when correctly compared through the laws of thermodynamics. Unless one measures heat and the biomolecules synthesized using ATP, it is inappropriate to assume that the only thing that counts in terms of food consumption and energy balance is the intake of dietary calories and weight storage.” (6)

And, as if all of this weren’t enough, the amount of usable energy that we do produce or use doesn’t say anything about where or what that energy is used for, which is vitally important to consider for both fat loss and health!

The Dangers of Caloric Restriction

The final false assumption of the calorie equation is that any excess energy we have will become fat, while any energy deficit will result in fat loss.

This assumption that fat gain is the product of excess energy and fat loss is the product of a lack of energy is probably the single most harmful misconception that exists in the health and nutrition field.

The 1st law of thermodynamics is often cited in support of this idea, which explains that energy cannot be created or destroyed. But, this has nothing to do with where energy is used or the physiological processes of fat gain and loss.

Energy is used for virtually everything we do. It’s used to accomplish our basic daily functions, like breathing and digesting, in addition to handling stressors, like exercise and mental work. Energy is also used to maintain, repair, and grow our tissues, like muscles, bones, fascia, and organs.

All the factors we’ve mentioned so far, including our hormonal state and the many aspects of our environment, determine the partitioning of energy, or where energy is used.

For example, in the rat study that was mentioned earlier, the amount of energy from consumed protein that was allocated to fat and muscle tissue differed based on the type of protein that was consumed (4).

However, the calorie equation doesn’t acknowledge the concept of energy partitioning and instead relies on the extremely common fallacy that any excess energy we have will be used for body fat and any energy deficit will come from body fat.

While this ignores a key physiological concept, there’s another problem with this fallacy that we haven’t addressed: body fat is a storage of fuel, or potential energy. In other words, the potential energy in food is stored as body fat when it’s NOT converted to usable energy.

While this is somewhat acknowledged, it’s assumed that energy production occurs until we have enough energy, at which point any potential energy left over becomes fat. But, that couldn’t be farther from the truth.

As was mentioned earlier, energy production, or mitochondrial respiration, is affected by all sorts of variables, from the amount of nutrients available to the time of day. When energy production is inhibited based on these many factors, the potential energy from our food is stored as fat and we’re left without enough energy to properly function.

This is what underlies fat gain and the obesity epidemic. Not too much energy, but too little energy (14).

As such, the recommendations to further reduce our available energy only make the problem worse, as is explained in this quote:

“In conclusion, the presented metabolic mechanism of environmentally caused obesity indicates energy deficiency as an engine working toward development of obesity. It is obvious that all efforts to stop this engine by further decreasing the energy cannot be successful. Thus, the low calorie diets and exercise regimens seem to be a redundant burden of already exhausted people.” (14)

Unfortunately, it doesn’t end there. Our bodies adapt to energy deficiencies by further inhibiting energy production and storing more fuel as fat in order to conserve energy, resulting in a vicious cycle (10, 14, 15).

This is the biggest reason why the calorie equation is destroying our health. We already lack energy due to the inhibition of mitochondrial respiration by nutrient deficiencies and many other problems, and then we eat less and exercise more, which further reduces the amount of energy we have available to properly function, encourages fat gain, and leads to the chronic diseases we see in epidemic proportions today.

We need to put an end to this terribly misguided approach to fat loss and health and instead shift our focus to the process of energy production. By increasing the amount of energy we produce, we can reduce the storage of food as body fat which will allow us to lose fat while also improving our health.

As I’m sure you’ve already gathered, there are quite a few factors affecting energy production. If you want to learn more about those factors and learn to lose fat the healthy way, sign up for the free mini-course below!

References

The Mythical Calorie Equation

Calories In – Calorie Out = Change in Body Fat

This ubiquitous equation represents the idea that the difference between the number of calories we consume and the number of calories we expend determines the amount of fat we gain or lose. It’s a wonderfully simple conception, although not an accurate one, and actually a very dangerous one.

It’s truly amazing to me that this equation has stuck around this long. The entire concept is illogical to begin with, not to mention the mounds of evidence against it.

Yet, the dogmatic adherence to this equation has informed so much of the current nutrition recommendations. This is especially true when it comes to fat loss, where “eat less and exercise more” is the common mantra. But it has also been applied to the general health recommendations to eat foods that are less calorie-dense, drink more water, and consume more protein and fiber to keep us full for longer, among many others.

While the fact that we associate calories with fat gain and loss is bad, the fact that we associate them with health is even worse.

But before we dive in too far, let’s start by exploring the extensive evidence that refutes the validity of equation.

Isocaloric Studies

If the calorie equation was valid, then consuming diets containing different foods with the same number of calories would have the same effects on body fat. But, many studies that have tested this hypothesis have shown that this isn’t the case. Let’s take a look at a few of them.

This first study, performed in a metabolic ward, had subjects on isocaloric reduced-fat or reduced-carbohydrate diets (1) (isocaloric means the diets had the same number of calories). They found that subjects on the reduced-fat diets lost more body fat than subjects on the reduced-carb diets. And, those on the reduced-fat diets lost less weight than those on the reduced-carb diets, meaning that a much higher percentage of the weight they lost was fat.

[This study also provides more evidence against the “burn fat for fat loss” fallacy, as those on the reduced-carb diets burned more fat than the reduced-fat group even though they lost less body fat.]

This next study also compared subjects on isocaloric diets with varying amounts of carbs and fat, although this one was performed on rats instead of humans (2). They found that the rats on the high-fat diets had higher total body fat by the end of the study than those on the control diet, but those on the high-carb diets didn’t. Again, remember that the high-fat and high-carb rats were fed the exact same number of calories!

In this study, human subjects were given 1 of 3 isocaloric diets that contained varying amounts of carbohydrates, and they found huge differences in weight loss, fat loss, and percent weight loss based on the amount of carbohydrates in the diet (3). In fact, those on the diet that was highest in carbohydrates lost 14 pounds more of body fat than those on the lowest carbohydrate diet during the 9-week intervention! In reference to these results, the authors commented that “no adequate explanation [could] be given for [the] weight loss differences.”

There are many more isocaloric studies that provide similar evidence against the calorie equation, including one on rats where two groups were fed the exact same diet except for the type of protein and ended up with a 26% difference in fat mass (4) and other studies showing that changing the amount of fat or carbohydrate in the diet affected the amount of body fat gained or lost, even when consuming the same number of calories (5, 6).

It’s clear based on these studies that the calorie equation isn’t quite as simple as it was made out to be. The types of foods that are eaten have a substantial effect on changes in body fat, rather than simply the number of “calories-in.”

Now, the argument can be made that changing the types of foods simply changes the number of “calories-out.” And, while this is true, it’s often entirely ignored in favor of the recommendations to simply “eat less and exercise more.”

Even when not ignored, the fact that the type of food, rather than simply the number of calories, affects the number of “calories-out” creates problems of its own.

It’s known that different diet compositions can vary in their metabolizable energy (the amount of energy in the food that’s actually digested and absorbed) and thermic effects (the amount of energy required for digesting and using the food). It’s also acknowledged that different diet compositions can cause changes in the resting metabolic rate and physical activity levels. But, some of the effects of different diet compositions can’t be fully explained yet.

This review, aimed at figuring out whether we can account for all the energetic effects of different diet compositions, looked at many calorie-controlled weight loss studies (7). They found that “neither macronutrient-specific differences in the availability of dietary energy nor changes in energy expenditure could explain [the] differences in weight loss” and concluded by suggesting that “further research is needed to identify the mechanisms that result in greater weight loss with one diet than with another.”

In other words, even if we account for differences in metabolizable energy, thermic effects, resting metabolic rate, and physical activity levels, (which very few people are doing) there are still unknown variables that would need to be factored in to make the calorie equation work.

This presents a glaring problem with this equation, but it doesn’t end here. There are other, more serious problems with the calorie equation that arise because it’s predicated on several false assumptions.

Caloric Restriction, Metabolic Adaptation, and Behavioral Compensation

The first of these assumptions is that our bodies’ energy usage doesn’t change based on our environment.

There have been many times where researchers have tried to apply the calorie equation to fat loss. They set up experiments where they reduce people’s food intakes and increase their exercise, thereby reducing the number of “calories-in” and increasing the number of “calories-out.”

And these studies do result in weight loss. But the amount of weight loss is nowhere near the amount predicted by the calorie equation.

This discrepancy boils down to two main factors:

1. Metabolic Adaptation

Metabolic adaptation is how our bodies internally adjust, or adapt, to changes in caloric intake (“calories-in”) or caloric expenditure (“calories-out”). When we reduce our caloric intake or increase our caloric expenditure, our bodies reduce the amount of energy they use. And when we increase our caloric intake or decrease our caloric expenditure, our bodies increase the amount of energy they use (8, 9, 10, 11).

This is accomplished through various hormonal and enzymatic changes, which allow for adjustments in energy usage, metabolic fuel selection, and energy partitioning.

These adaptive responses throw another wrench in the calorie equation. If we factor metabolic adaptation into the equation, we would have to reduce our caloric intake even more to achieve our desired weight loss.

2. Behavioral Compensation

Behavioral compensation is how we respond externally to changes in caloric intake or expenditure. This could mean reducing the amount we exercise when we eat fewer calories or increasing the amount we eat when we exercise more.

One review that considered many weight loss studies found that, because of behavioral compensation, the amount of weight loss from caloric restriction averages to be 12-44% less than what’s predicted by the calorie equation (12). They also found the amount of weight loss from increased exercise to be 55-64% less than was expected due to behavioral compensation.

Those are HUGE differences between the mythical calorie equation and reality!

And, behavioral compensation is an even bigger factor when we increase the amount of “calories-in.” The amount of weight gain in these situations is up to 96% less than is expected from the calorie equation! (12) You read that right, 96%! That basically means that we’re really good at compensating when we eat more food than normal, to the point that it’s pretty hard to gain weight that way.

But of course, metabolic adaptation and behavioral compensation don’t mean that the mythical equation is wrong. They’re just two more variables we have to factor into the equation that at this point is unrecognizable compared to the original “calories in – calories out = change in body fat.”

Up until this point we’ve only been dealing with adjustments to the calorie equation, but after considering this next false assumption it’ll become quite clear that this equation has no place in the health or fat loss arena.

What Are Calories?

This brings us to one of the most egregious errors that underlies the calorie equation: Calories are not relevant to human physiology.

Calories are simply a measure of energy, specifically heat energy.

In the context of nutrition, we think about the number of calories, or potential energy, held in certain foods. But, we can consider the number of calories in anything, whether it’s grass, wood, or gasoline.

Now, we all know that our bodies can’t convert the energy (calories) in grass, wood, or gasoline to usable energy in our bodies. So why do we assume that we’ll equally convert the energy in all food to usable energy in our bodies?

We consider that a mango has 200 calories, a steak has 600 calories, and a doughnut has 300 calories, but we don’t consider how much of that potential energy can or will be converted to usable energy.

There are many factors that affect how much of the energy, or calories, in the food we eat will become usable energy in our bodies.

The food must first be digested and absorbed. However, the amount of the food that actually gets digested and absorbed varies greatly based on the food and our gut function, and varying amounts of energy are required for this digestion and absorption.

Once absorbed, the carbohydrates, fats, and protein from the food we eat can be used to produce energy. This occurs in the mitochondria of our cells through a process called respiration.

During this process, the food we eat is converted into a form of usable energy that’s held in a molecule called ATP. But, there are tons of factors that affect whether the carbohydrates, fats, and protein even get to the mitochondria, let alone whether they’ll be used to produce ATP.

The different macronutrients (carbs, fats, and protein) vary significantly in this regard. Carbohydrates are our primary energy source while fat is our secondary energy source. Protein, on the other hand, is not likely to be converted to usable energy through mitochondrial respiration and is instead used primarily for building and rebuilding tissues.

So, it makes little sense to equate the potential energy, or calories, between the different macronutrients, as the likelihood that they’ll be used to produce ATP varies considerably. Equating the calories between the different macronutrients actually violates the second law of thermodynamics, as is explained here:

“A review of simple thermodynamic principles shows that weight change on isocaloric diets is not expected to be independent of path (metabolism of macronutrients) and indeed such a general principle would be a violation of the second law [of thermodynamics].” “The second law of thermodynamics says that variation of efficiency for different metabolic pathways is to be expected. Thus, ironically the dictum that a “calorie is a calorie” violates the second law of thermodynamics, as a matter of principle.” (13)

And, the factors that affect mitochondrial respiration go far beyond the differences between macronutrients. They also include the hormonal state, the amount of nutrients available, the toxins present, the time of day, the ambient temperature, the amount of sunlight present, the psychological state, and virtually every other aspect of our environment.

In other words, our bodies don’t run on a calorie currency, as they must convert the energy in food that we call “calories” into energy that they can use. And the amount of calories in our food is barely relevant considering the many factors that affect its conversion to usable energy.

The problems with the misplaced focus on calories has been nicely summed up in this quote:

“It is increasingly clear that the idea that “a calorie is a calorie” is misleading… Different diets… lead to different biochemical pathways (due to the hormonal and enzymatic changes) that are not equivalent when correctly compared through the laws of thermodynamics. Unless one measures heat and the biomolecules synthesized using ATP, it is inappropriate to assume that the only thing that counts in terms of food consumption and energy balance is the intake of dietary calories and weight storage.” (6)

And, as if all of this weren’t enough, the amount of usable energy that we do produce or use doesn’t say anything about where or what that energy is used for, which is vitally important to consider for both fat loss and health!

The Dangers of Caloric Restriction

The final false assumption of the calorie equation is that any excess energy we have will become fat, while any energy deficit will result in fat loss.

This assumption that fat gain is the product of excess energy and fat loss is the product of a lack of energy is probably the single most harmful misconception that exists in the health and nutrition field.

The 1st law of thermodynamics is often cited in support of this idea, which explains that energy cannot be created or destroyed. But, this has nothing to do with where energy is used or the physiological processes of fat gain and loss.

Energy is used for virtually everything we do. It’s used to accomplish our basic daily functions, like breathing and digesting, in addition to handling stressors, like exercise and mental work. Energy is also used to maintain, repair, and grow our tissues, like muscles, bones, fascia, and organs.

All the factors we’ve mentioned so far, including our hormonal state and the many aspects of our environment, determine the partitioning of energy, or where energy is used.

For example, in the rat study that was mentioned earlier, the amount of energy from consumed protein that was allocated to fat and muscle tissue differed based on the type of protein that was consumed (4).

However, the calorie equation doesn’t acknowledge the concept of energy partitioning and instead relies on the extremely common fallacy that any excess energy we have will be used for body fat and any energy deficit will come from body fat.

While this ignores a key physiological concept, there’s another problem with this fallacy that we haven’t addressed: body fat is a storage of fuel, or potential energy. In other words, the potential energy in food is stored as body fat when it’s NOT converted to usable energy.

While this is somewhat acknowledged, it’s assumed that energy production occurs until we have enough energy, at which point any potential energy left over becomes fat. But, that couldn’t be farther from the truth.

As was mentioned earlier, energy production, or mitochondrial respiration, is affected by all sorts of variables, from the amount of nutrients available to the time of day. When energy production is inhibited based on these many factors, the potential energy from our food is stored as fat and we’re left without enough energy to properly function.

This is what underlies fat gain and the obesity epidemic. Not too much energy, but too little energy (14).

As such, the recommendations to further reduce our available energy only make the problem worse, as is explained in this quote:

“In conclusion, the presented metabolic mechanism of environmentally caused obesity indicates energy deficiency as an engine working toward development of obesity. It is obvious that all efforts to stop this engine by further decreasing the energy cannot be successful. Thus, the low calorie diets and exercise regimens seem to be a redundant burden of already exhausted people.” (14)

Unfortunately, it doesn’t end there. Our bodies adapt to energy deficiencies by further inhibiting energy production and storing more fuel as fat in order to conserve energy, resulting in a vicious cycle (10, 14, 15).

This is the biggest reason why the calorie equation is destroying our health. We already lack energy due to the inhibition of mitochondrial respiration by nutrient deficiencies and many other problems, and then we eat less and exercise more, which further reduces the amount of energy we have available to properly function, encourages fat gain, and leads to the chronic diseases we see in epidemic proportions today.

We need to put an end to this terribly misguided approach to fat loss and health and instead shift our focus to the process of energy production. By increasing the amount of energy we produce, we can reduce the storage of food as body fat which will allow us to lose fat while also improving our health.

As I’m sure you’ve already gathered, there are quite a few factors affecting energy production. If you want to learn more about those factors and learn to lose fat the healthy way, sign up for the free mini-course below!

References

The Mythical Calorie Equation

Calories In – Calorie Out = Change in Body Fat

This ubiquitous equation represents the idea that the difference between the number of calories we consume and the number of calories we expend determines the amount of fat we gain or lose. It’s a wonderfully simple conception, although not an accurate one, and actually a very dangerous one.

It’s truly amazing to me that this equation has stuck around this long. The entire concept is illogical to begin with, not to mention the mounds of evidence against it.

Yet, the dogmatic adherence to this equation has informed so much of the current nutrition recommendations. This is especially true when it comes to fat loss, where “eat less and exercise more” is the common mantra. But it has also been applied to the general health recommendations to eat foods that are less calorie-dense, drink more water, and consume more protein and fiber to keep us full for longer, among many others.

While the fact that we associate calories with fat gain and loss is bad, the fact that we associate them with health is even worse.

But before we dive in too far, let’s start by exploring the extensive evidence that refutes the validity of equation.

Isocaloric Studies

If the calorie equation was valid, then consuming diets containing different foods with the same number of calories would have the same effects on body fat. But, many studies that have tested this hypothesis have shown that this isn’t the case. Let’s take a look at a few of them.

This first study, performed in a metabolic ward, had subjects on isocaloric reduced-fat or reduced-carbohydrate diets (1) (isocaloric means the diets had the same number of calories). They found that subjects on the reduced-fat diets lost more body fat than subjects on the reduced-carb diets. And, those on the reduced-fat diets lost less weight than those on the reduced-carb diets, meaning that a much higher percentage of the weight they lost was fat.

[This study also provides more evidence against the “burn fat for fat loss” fallacy, as those on the reduced-carb diets burned more fat than the reduced-fat group even though they lost less body fat.]

This next study also compared subjects on isocaloric diets with varying amounts of carbs and fat, although this one was performed on rats instead of humans (2). They found that the rats on the high-fat diets had higher total body fat by the end of the study than those on the control diet, but those on the high-carb diets didn’t. Again, remember that the high-fat and high-carb rats were fed the exact same number of calories!

In this study, human subjects were given 1 of 3 isocaloric diets that contained varying amounts of carbohydrates, and they found huge differences in weight loss, fat loss, and percent weight loss based on the amount of carbohydrates in the diet (3). In fact, those on the diet that was highest in carbohydrates lost 14 pounds more of body fat than those on the lowest carbohydrate diet during the 9-week intervention! In reference to these results, the authors commented that “no adequate explanation [could] be given for [the] weight loss differences.”

There are many more isocaloric studies that provide similar evidence against the calorie equation, including one on rats where two groups were fed the exact same diet except for the type of protein and ended up with a 26% difference in fat mass (4) and other studies showing that changing the amount of fat or carbohydrate in the diet affected the amount of body fat gained or lost, even when consuming the same number of calories (5, 6).

It’s clear based on these studies that the calorie equation isn’t quite as simple as it was made out to be. The types of foods that are eaten have a substantial effect on changes in body fat, rather than simply the number of “calories-in.”

Now, the argument can be made that changing the types of foods simply changes the number of “calories-out.” And, while this is true, it’s often entirely ignored in favor of the recommendations to simply “eat less and exercise more.”

Even when not ignored, the fact that the type of food, rather than simply the number of calories, affects the number of “calories-out” creates problems of its own.

It’s known that different diet compositions can vary in their metabolizable energy (the amount of energy in the food that’s actually digested and absorbed) and thermic effects (the amount of energy required for digesting and using the food). It’s also acknowledged that different diet compositions can cause changes in the resting metabolic rate and physical activity levels. But, some of the effects of different diet compositions can’t be fully explained yet.

This review, aimed at figuring out whether we can account for all the energetic effects of different diet compositions, looked at many calorie-controlled weight loss studies (7). They found that “neither macronutrient-specific differences in the availability of dietary energy nor changes in energy expenditure could explain [the] differences in weight loss” and concluded by suggesting that “further research is needed to identify the mechanisms that result in greater weight loss with one diet than with another.”

In other words, even if we account for differences in metabolizable energy, thermic effects, resting metabolic rate, and physical activity levels, (which very few people are doing) there are still unknown variables that would need to be factored in to make the calorie equation work.

This presents a glaring problem with this equation, but it doesn’t end here. There are other, more serious problems with the calorie equation that arise because it’s predicated on several false assumptions.

Caloric Restriction, Metabolic Adaptation, and Behavioral Compensation

The first of these assumptions is that our bodies’ energy usage doesn’t change based on our environment.

There have been many times where researchers have tried to apply the calorie equation to fat loss. They set up experiments where they reduce people’s food intakes and increase their exercise, thereby reducing the number of “calories-in” and increasing the number of “calories-out.”

And these studies do result in weight loss. But the amount of weight loss is nowhere near the amount predicted by the calorie equation.

This discrepancy boils down to two main factors:

1. Metabolic Adaptation

Metabolic adaptation is how our bodies internally adjust, or adapt, to changes in caloric intake (“calories-in”) or caloric expenditure (“calories-out”). When we reduce our caloric intake or increase our caloric expenditure, our bodies reduce the amount of energy they use. And when we increase our caloric intake or decrease our caloric expenditure, our bodies increase the amount of energy they use (8, 9, 10, 11).

This is accomplished through various hormonal and enzymatic changes, which allow for adjustments in energy usage, metabolic fuel selection, and energy partitioning.

These adaptive responses throw another wrench in the calorie equation. If we factor metabolic adaptation into the equation, we would have to reduce our caloric intake even more to achieve our desired weight loss.

2. Behavioral Compensation

Behavioral compensation is how we respond externally to changes in caloric intake or expenditure. This could mean reducing the amount we exercise when we eat fewer calories or increasing the amount we eat when we exercise more.

One review that considered many weight loss studies found that, because of behavioral compensation, the amount of weight loss from caloric restriction averages to be 12-44% less than what’s predicted by the calorie equation (12). They also found the amount of weight loss from increased exercise to be 55-64% less than was expected due to behavioral compensation.

Those are HUGE differences between the mythical calorie equation and reality!

And, behavioral compensation is an even bigger factor when we increase the amount of “calories-in.” The amount of weight gain in these situations is up to 96% less than is expected from the calorie equation! (12) You read that right, 96%! That basically means that we’re really good at compensating when we eat more food than normal, to the point that it’s pretty hard to gain weight that way.

But of course, metabolic adaptation and behavioral compensation don’t mean that the mythical equation is wrong. They’re just two more variables we have to factor into the equation that at this point is unrecognizable compared to the original “calories in – calories out = change in body fat.”

Up until this point we’ve only been dealing with adjustments to the calorie equation, but after considering this next false assumption it’ll become quite clear that this equation has no place in the health or fat loss arena.

What Are Calories?

This brings us to one of the most egregious errors that underlies the calorie equation: Calories are not relevant to human physiology.

Calories are simply a measure of energy, specifically heat energy.

In the context of nutrition, we think about the number of calories, or potential energy, held in certain foods. But, we can consider the number of calories in anything, whether it’s grass, wood, or gasoline.

Now, we all know that our bodies can’t convert the energy (calories) in grass, wood, or gasoline to usable energy in our bodies. So why do we assume that we’ll equally convert the energy in all food to usable energy in our bodies?

We consider that a mango has 200 calories, a steak has 600 calories, and a doughnut has 300 calories, but we don’t consider how much of that potential energy can or will be converted to usable energy.

There are many factors that affect how much of the energy, or calories, in the food we eat will become usable energy in our bodies.

The food must first be digested and absorbed. However, the amount of the food that actually gets digested and absorbed varies greatly based on the food and our gut function, and varying amounts of energy are required for this digestion and absorption.

Once absorbed, the carbohydrates, fats, and protein from the food we eat can be used to produce energy. This occurs in the mitochondria of our cells through a process called respiration.

During this process, the food we eat is converted into a form of usable energy that’s held in a molecule called ATP. But, there are tons of factors that affect whether the carbohydrates, fats, and protein even get to the mitochondria, let alone whether they’ll be used to produce ATP.

The different macronutrients (carbs, fats, and protein) vary significantly in this regard. Carbohydrates are our primary energy source while fat is our secondary energy source. Protein, on the other hand, is not likely to be converted to usable energy through mitochondrial respiration and is instead used primarily for building and rebuilding tissues.

So, it makes little sense to equate the potential energy, or calories, between the different macronutrients, as the likelihood that they’ll be used to produce ATP varies considerably. Equating the calories between the different macronutrients actually violates the second law of thermodynamics, as is explained here:

“A review of simple thermodynamic principles shows that weight change on isocaloric diets is not expected to be independent of path (metabolism of macronutrients) and indeed such a general principle would be a violation of the second law [of thermodynamics].” “The second law of thermodynamics says that variation of efficiency for different metabolic pathways is to be expected. Thus, ironically the dictum that a “calorie is a calorie” violates the second law of thermodynamics, as a matter of principle.” (13)

And, the factors that affect mitochondrial respiration go far beyond the differences between macronutrients. They also include the hormonal state, the amount of nutrients available, the toxins present, the time of day, the ambient temperature, the amount of sunlight present, the psychological state, and virtually every other aspect of our environment.

In other words, our bodies don’t run on a calorie currency, as they must convert the energy in food that we call “calories” into energy that they can use. And the amount of calories in our food is barely relevant considering the many factors that affect its conversion to usable energy.

The problems with the misplaced focus on calories has been nicely summed up in this quote:

“It is increasingly clear that the idea that “a calorie is a calorie” is misleading… Different diets… lead to different biochemical pathways (due to the hormonal and enzymatic changes) that are not equivalent when correctly compared through the laws of thermodynamics. Unless one measures heat and the biomolecules synthesized using ATP, it is inappropriate to assume that the only thing that counts in terms of food consumption and energy balance is the intake of dietary calories and weight storage.” (6)

And, as if all of this weren’t enough, the amount of usable energy that we do produce or use doesn’t say anything about where or what that energy is used for, which is vitally important to consider for both fat loss and health!

The Dangers of Caloric Restriction

The final false assumption of the calorie equation is that any excess energy we have will become fat, while any energy deficit will result in fat loss.

This assumption that fat gain is the product of excess energy and fat loss is the product of a lack of energy is probably the single most harmful misconception that exists in the health and nutrition field.

The 1st law of thermodynamics is often cited in support of this idea, which explains that energy cannot be created or destroyed. But, this has nothing to do with where energy is used or the physiological processes of fat gain and loss.

Energy is used for virtually everything we do. It’s used to accomplish our basic daily functions, like breathing and digesting, in addition to handling stressors, like exercise and mental work. Energy is also used to maintain, repair, and grow our tissues, like muscles, bones, fascia, and organs.

All the factors we’ve mentioned so far, including our hormonal state and the many aspects of our environment, determine the partitioning of energy, or where energy is used.

For example, in the rat study that was mentioned earlier, the amount of energy from consumed protein that was allocated to fat and muscle tissue differed based on the type of protein that was consumed (4).

However, the calorie equation doesn’t acknowledge the concept of energy partitioning and instead relies on the extremely common fallacy that any excess energy we have will be used for body fat and any energy deficit will come from body fat.

While this ignores a key physiological concept, there’s another problem with this fallacy that we haven’t addressed: body fat is a storage of fuel, or potential energy. In other words, the potential energy in food is stored as body fat when it’s NOT converted to usable energy.

While this is somewhat acknowledged, it’s assumed that energy production occurs until we have enough energy, at which point any potential energy left over becomes fat. But, that couldn’t be farther from the truth.

As was mentioned earlier, energy production, or mitochondrial respiration, is affected by all sorts of variables, from the amount of nutrients available to the time of day. When energy production is inhibited based on these many factors, the potential energy from our food is stored as fat and we’re left without enough energy to properly function.

This is what underlies fat gain and the obesity epidemic. Not too much energy, but too little energy (14).

As such, the recommendations to further reduce our available energy only make the problem worse, as is explained in this quote:

“In conclusion, the presented metabolic mechanism of environmentally caused obesity indicates energy deficiency as an engine working toward development of obesity. It is obvious that all efforts to stop this engine by further decreasing the energy cannot be successful. Thus, the low calorie diets and exercise regimens seem to be a redundant burden of already exhausted people.” (14)

Unfortunately, it doesn’t end there. Our bodies adapt to energy deficiencies by further inhibiting energy production and storing more fuel as fat in order to conserve energy, resulting in a vicious cycle (10, 14, 15).

This is the biggest reason why the calorie equation is destroying our health. We already lack energy due to the inhibition of mitochondrial respiration by nutrient deficiencies and many other problems, and then we eat less and exercise more, which further reduces the amount of energy we have available to properly function, encourages fat gain, and leads to the chronic diseases we see in epidemic proportions today.

We need to put an end to this terribly misguided approach to fat loss and health and instead shift our focus to the process of energy production. By increasing the amount of energy we produce, we can reduce the storage of food as body fat which will allow us to lose fat while also improving our health.

As I’m sure you’ve already gathered, there are quite a few factors affecting energy production. If you want to learn more about those factors and learn to lose fat the healthy way, sign up for the free mini-course below!

References

The Mythical Calorie Equation

Calories In – Calorie Out = Change in Body Fat

This ubiquitous equation represents the idea that the difference between the number of calories we consume and the number of calories we expend determines the amount of fat we gain or lose. It’s a wonderfully simple conception, although not an accurate one, and actually a very dangerous one.

It’s truly amazing to me that this equation has stuck around this long. The entire concept is illogical to begin with, not to mention the mounds of evidence against it.

Yet, the dogmatic adherence to this equation has informed so much of the current nutrition recommendations. This is especially true when it comes to fat loss, where “eat less and exercise more” is the common mantra. But it has also been applied to the general health recommendations to eat foods that are less calorie-dense, drink more water, and consume more protein and fiber to keep us full for longer, among many others.

While the fact that we associate calories with fat gain and loss is bad, the fact that we associate them with health is even worse.

But before we dive in too far, let’s start by exploring the extensive evidence that refutes the validity of equation.

Isocaloric Studies

If the calorie equation was valid, then consuming diets containing different foods with the same number of calories would have the same effects on body fat. But, many studies that have tested this hypothesis have shown that this isn’t the case. Let’s take a look at a few of them.

This first study, performed in a metabolic ward, had subjects on isocaloric reduced-fat or reduced-carbohydrate diets (1) (isocaloric means the diets had the same number of calories). They found that subjects on the reduced-fat diets lost more body fat than subjects on the reduced-carb diets. And, those on the reduced-fat diets lost less weight than those on the reduced-carb diets, meaning that a much higher percentage of the weight they lost was fat.

[This study also provides more evidence against the “burn fat for fat loss” fallacy, as those on the reduced-carb diets burned more fat than the reduced-fat group even though they lost less body fat.]

This next study also compared subjects on isocaloric diets with varying amounts of carbs and fat, although this one was performed on rats instead of humans (2). They found that the rats on the high-fat diets had higher total body fat by the end of the study than those on the control diet, but those on the high-carb diets didn’t. Again, remember that the high-fat and high-carb rats were fed the exact same number of calories!

In this study, human subjects were given 1 of 3 isocaloric diets that contained varying amounts of carbohydrates, and they found huge differences in weight loss, fat loss, and percent weight loss based on the amount of carbohydrates in the diet (3). In fact, those on the diet that was highest in carbohydrates lost 14 pounds more of body fat than those on the lowest carbohydrate diet during the 9-week intervention! In reference to these results, the authors commented that “no adequate explanation [could] be given for [the] weight loss differences.”

There are many more isocaloric studies that provide similar evidence against the calorie equation, including one on rats where two groups were fed the exact same diet except for the type of protein and ended up with a 26% difference in fat mass (4) and other studies showing that changing the amount of fat or carbohydrate in the diet affected the amount of body fat gained or lost, even when consuming the same number of calories (5, 6).

It’s clear based on these studies that the calorie equation isn’t quite as simple as it was made out to be. The types of foods that are eaten have a substantial effect on changes in body fat, rather than simply the number of “calories-in.”

Now, the argument can be made that changing the types of foods simply changes the number of “calories-out.” And, while this is true, it’s often entirely ignored in favor of the recommendations to simply “eat less and exercise more.”

Even when not ignored, the fact that the type of food, rather than simply the number of calories, affects the number of “calories-out” creates problems of its own.

It’s known that different diet compositions can vary in their metabolizable energy (the amount of energy in the food that’s actually digested and absorbed) and thermic effects (the amount of energy required for digesting and using the food). It’s also acknowledged that different diet compositions can cause changes in the resting metabolic rate and physical activity levels. But, some of the effects of different diet compositions can’t be fully explained yet.

This review, aimed at figuring out whether we can account for all the energetic effects of different diet compositions, looked at many calorie-controlled weight loss studies (7). They found that “neither macronutrient-specific differences in the availability of dietary energy nor changes in energy expenditure could explain [the] differences in weight loss” and concluded by suggesting that “further research is needed to identify the mechanisms that result in greater weight loss with one diet than with another.”

In other words, even if we account for differences in metabolizable energy, thermic effects, resting metabolic rate, and physical activity levels, (which very few people are doing) there are still unknown variables that would need to be factored in to make the calorie equation work.

This presents a glaring problem with this equation, but it doesn’t end here. There are other, more serious problems with the calorie equation that arise because it’s predicated on several false assumptions.

Caloric Restriction, Metabolic Adaptation, and Behavioral Compensation

The first of these assumptions is that our bodies’ energy usage doesn’t change based on our environment.

There have been many times where researchers have tried to apply the calorie equation to fat loss. They set up experiments where they reduce people’s food intakes and increase their exercise, thereby reducing the number of “calories-in” and increasing the number of “calories-out.”

And these studies do result in weight loss. But the amount of weight loss is nowhere near the amount predicted by the calorie equation.

This discrepancy boils down to two main factors:

1. Metabolic Adaptation

Metabolic adaptation is how our bodies internally adjust, or adapt, to changes in caloric intake (“calories-in”) or caloric expenditure (“calories-out”). When we reduce our caloric intake or increase our caloric expenditure, our bodies reduce the amount of energy they use. And when we increase our caloric intake or decrease our caloric expenditure, our bodies increase the amount of energy they use (8, 9, 10, 11).

This is accomplished through various hormonal and enzymatic changes, which allow for adjustments in energy usage, metabolic fuel selection, and energy partitioning.

These adaptive responses throw another wrench in the calorie equation. If we factor metabolic adaptation into the equation, we would have to reduce our caloric intake even more to achieve our desired weight loss.

2. Behavioral Compensation

Behavioral compensation is how we respond externally to changes in caloric intake or expenditure. This could mean reducing the amount we exercise when we eat fewer calories or increasing the amount we eat when we exercise more.

One review that considered many weight loss studies found that, because of behavioral compensation, the amount of weight loss from caloric restriction averages to be 12-44% less than what’s predicted by the calorie equation (12). They also found the amount of weight loss from increased exercise to be 55-64% less than was expected due to behavioral compensation.

Those are HUGE differences between the mythical calorie equation and reality!

And, behavioral compensation is an even bigger factor when we increase the amount of “calories-in.” The amount of weight gain in these situations is up to 96% less than is expected from the calorie equation! (12) You read that right, 96%! That basically means that we’re really good at compensating when we eat more food than normal, to the point that it’s pretty hard to gain weight that way.

But of course, metabolic adaptation and behavioral compensation don’t mean that the mythical equation is wrong. They’re just two more variables we have to factor into the equation that at this point is unrecognizable compared to the original “calories in – calories out = change in body fat.”

Up until this point we’ve only been dealing with adjustments to the calorie equation, but after considering this next false assumption it’ll become quite clear that this equation has no place in the health or fat loss arena.

What Are Calories?

This brings us to one of the most egregious errors that underlies the calorie equation: Calories are not relevant to human physiology.

Calories are simply a measure of energy, specifically heat energy.

In the context of nutrition, we think about the number of calories, or potential energy, held in certain foods. But, we can consider the number of calories in anything, whether it’s grass, wood, or gasoline.

Now, we all know that our bodies can’t convert the energy (calories) in grass, wood, or gasoline to usable energy in our bodies. So why do we assume that we’ll equally convert the energy in all food to usable energy in our bodies?

We consider that a mango has 200 calories, a steak has 600 calories, and a doughnut has 300 calories, but we don’t consider how much of that potential energy can or will be converted to usable energy.

There are many factors that affect how much of the energy, or calories, in the food we eat will become usable energy in our bodies.

The food must first be digested and absorbed. However, the amount of the food that actually gets digested and absorbed varies greatly based on the food and our gut function, and varying amounts of energy are required for this digestion and absorption.

Once absorbed, the carbohydrates, fats, and protein from the food we eat can be used to produce energy. This occurs in the mitochondria of our cells through a process called respiration.

During this process, the food we eat is converted into a form of usable energy that’s held in a molecule called ATP. But, there are tons of factors that affect whether the carbohydrates, fats, and protein even get to the mitochondria, let alone whether they’ll be used to produce ATP.

The different macronutrients (carbs, fats, and protein) vary significantly in this regard. Carbohydrates are our primary energy source while fat is our secondary energy source. Protein, on the other hand, is not likely to be converted to usable energy through mitochondrial respiration and is instead used primarily for building and rebuilding tissues.

So, it makes little sense to equate the potential energy, or calories, between the different macronutrients, as the likelihood that they’ll be used to produce ATP varies considerably. Equating the calories between the different macronutrients actually violates the second law of thermodynamics, as is explained here:

“A review of simple thermodynamic principles shows that weight change on isocaloric diets is not expected to be independent of path (metabolism of macronutrients) and indeed such a general principle would be a violation of the second law [of thermodynamics].” “The second law of thermodynamics says that variation of efficiency for different metabolic pathways is to be expected. Thus, ironically the dictum that a “calorie is a calorie” violates the second law of thermodynamics, as a matter of principle.” (13)

And, the factors that affect mitochondrial respiration go far beyond the differences between macronutrients. They also include the hormonal state, the amount of nutrients available, the toxins present, the time of day, the ambient temperature, the amount of sunlight present, the psychological state, and virtually every other aspect of our environment.

In other words, our bodies don’t run on a calorie currency, as they must convert the energy in food that we call “calories” into energy that they can use. And the amount of calories in our food is barely relevant considering the many factors that affect its conversion to usable energy.

The problems with the misplaced focus on calories has been nicely summed up in this quote:

“It is increasingly clear that the idea that “a calorie is a calorie” is misleading… Different diets… lead to different biochemical pathways (due to the hormonal and enzymatic changes) that are not equivalent when correctly compared through the laws of thermodynamics. Unless one measures heat and the biomolecules synthesized using ATP, it is inappropriate to assume that the only thing that counts in terms of food consumption and energy balance is the intake of dietary calories and weight storage.” (6)

And, as if all of this weren’t enough, the amount of usable energy that we do produce or use doesn’t say anything about where or what that energy is used for, which is vitally important to consider for both fat loss and health!

The Dangers of Caloric Restriction

The final false assumption of the calorie equation is that any excess energy we have will become fat, while any energy deficit will result in fat loss.

This assumption that fat gain is the product of excess energy and fat loss is the product of a lack of energy is probably the single most harmful misconception that exists in the health and nutrition field.

The 1st law of thermodynamics is often cited in support of this idea, which explains that energy cannot be created or destroyed. But, this has nothing to do with where energy is used or the physiological processes of fat gain and loss.

Energy is used for virtually everything we do. It’s used to accomplish our basic daily functions, like breathing and digesting, in addition to handling stressors, like exercise and mental work. Energy is also used to maintain, repair, and grow our tissues, like muscles, bones, fascia, and organs.

All the factors we’ve mentioned so far, including our hormonal state and the many aspects of our environment, determine the partitioning of energy, or where energy is used.

For example, in the rat study that was mentioned earlier, the amount of energy from consumed protein that was allocated to fat and muscle tissue differed based on the type of protein that was consumed (4).

However, the calorie equation doesn’t acknowledge the concept of energy partitioning and instead relies on the extremely common fallacy that any excess energy we have will be used for body fat and any energy deficit will come from body fat.

While this ignores a key physiological concept, there’s another problem with this fallacy that we haven’t addressed: body fat is a storage of fuel, or potential energy. In other words, the potential energy in food is stored as body fat when it’s NOT converted to usable energy.

While this is somewhat acknowledged, it’s assumed that energy production occurs until we have enough energy, at which point any potential energy left over becomes fat. But, that couldn’t be farther from the truth.

As was mentioned earlier, energy production, or mitochondrial respiration, is affected by all sorts of variables, from the amount of nutrients available to the time of day. When energy production is inhibited based on these many factors, the potential energy from our food is stored as fat and we’re left without enough energy to properly function.

This is what underlies fat gain and the obesity epidemic. Not too much energy, but too little energy (14).

As such, the recommendations to further reduce our available energy only make the problem worse, as is explained in this quote:

“In conclusion, the presented metabolic mechanism of environmentally caused obesity indicates energy deficiency as an engine working toward development of obesity. It is obvious that all efforts to stop this engine by further decreasing the energy cannot be successful. Thus, the low calorie diets and exercise regimens seem to be a redundant burden of already exhausted people.” (14)

Unfortunately, it doesn’t end there. Our bodies adapt to energy deficiencies by further inhibiting energy production and storing more fuel as fat in order to conserve energy, resulting in a vicious cycle (10, 14, 15).

This is the biggest reason why the calorie equation is destroying our health. We already lack energy due to the inhibition of mitochondrial respiration by nutrient deficiencies and many other problems, and then we eat less and exercise more, which further reduces the amount of energy we have available to properly function, encourages fat gain, and leads to the chronic diseases we see in epidemic proportions today.

We need to put an end to this terribly misguided approach to fat loss and health and instead shift our focus to the process of energy production. By increasing the amount of energy we produce, we can reduce the storage of food as body fat which will allow us to lose fat while also improving our health.

As I’m sure you’ve already gathered, there are quite a few factors affecting energy production. If you want to learn more about those factors and learn to lose fat the healthy way, sign up for the free mini-course below!

References

The Mythical Calorie Equation

Calories In – Calorie Out = Change in Body Fat

This ubiquitous equation represents the idea that the difference between the number of calories we consume and the number of calories we expend determines the amount of fat we gain or lose. It’s a wonderfully simple conception, although not an accurate one, and actually a very dangerous one.

It’s truly amazing to me that this equation has stuck around this long. The entire concept is illogical to begin with, not to mention the mounds of evidence against it.

Yet, the dogmatic adherence to this equation has informed so much of the current nutrition recommendations. This is especially true when it comes to fat loss, where “eat less and exercise more” is the common mantra. But it has also been applied to the general health recommendations to eat foods that are less calorie-dense, drink more water, and consume more protein and fiber to keep us full for longer, among many others.

While the fact that we associate calories with fat gain and loss is bad, the fact that we associate them with health is even worse.

But before we dive in too far, let’s start by exploring the extensive evidence that refutes the validity of equation.

Isocaloric Studies

If the calorie equation was valid, then consuming diets containing different foods with the same number of calories would have the same effects on body fat. But, many studies that have tested this hypothesis have shown that this isn’t the case. Let’s take a look at a few of them.

This first study, performed in a metabolic ward, had subjects on isocaloric reduced-fat or reduced-carbohydrate diets (1) (isocaloric means the diets had the same number of calories). They found that subjects on the reduced-fat diets lost more body fat than subjects on the reduced-carb diets. And, those on the reduced-fat diets lost less weight than those on the reduced-carb diets, meaning that a much higher percentage of the weight they lost was fat.

[This study also provides more evidence against the “burn fat for fat loss” fallacy, as those on the reduced-carb diets burned more fat than the reduced-fat group even though they lost less body fat.]

This next study also compared subjects on isocaloric diets with varying amounts of carbs and fat, although this one was performed on rats instead of humans (2). They found that the rats on the high-fat diets had higher total body fat by the end of the study than those on the control diet, but those on the high-carb diets didn’t. Again, remember that the high-fat and high-carb rats were fed the exact same number of calories!

In this study, human subjects were given 1 of 3 isocaloric diets that contained varying amounts of carbohydrates, and they found huge differences in weight loss, fat loss, and percent weight loss based on the amount of carbohydrates in the diet (3). In fact, those on the diet that was highest in carbohydrates lost 14 pounds more of body fat than those on the lowest carbohydrate diet during the 9-week intervention! In reference to these results, the authors commented that “no adequate explanation [could] be given for [the] weight loss differences.”

There are many more isocaloric studies that provide similar evidence against the calorie equation, including one on rats where two groups were fed the exact same diet except for the type of protein and ended up with a 26% difference in fat mass (4) and other studies showing that changing the amount of fat or carbohydrate in the diet affected the amount of body fat gained or lost, even when consuming the same number of calories (5, 6).

It’s clear based on these studies that the calorie equation isn’t quite as simple as it was made out to be. The types of foods that are eaten have a substantial effect on changes in body fat, rather than simply the number of “calories-in.”

Now, the argument can be made that changing the types of foods simply changes the number of “calories-out.” And, while this is true, it’s often entirely ignored in favor of the recommendations to simply “eat less and exercise more.”

Even when not ignored, the fact that the type of food, rather than simply the number of calories, affects the number of “calories-out” creates problems of its own.

It’s known that different diet compositions can vary in their metabolizable energy (the amount of energy in the food that’s actually digested and absorbed) and thermic effects (the amount of energy required for digesting and using the food). It’s also acknowledged that different diet compositions can cause changes in the resting metabolic rate and physical activity levels. But, some of the effects of different diet compositions can’t be fully explained yet.

This review, aimed at figuring out whether we can account for all the energetic effects of different diet compositions, looked at many calorie-controlled weight loss studies (7). They found that “neither macronutrient-specific differences in the availability of dietary energy nor changes in energy expenditure could explain [the] differences in weight loss” and concluded by suggesting that “further research is needed to identify the mechanisms that result in greater weight loss with one diet than with another.”

In other words, even if we account for differences in metabolizable energy, thermic effects, resting metabolic rate, and physical activity levels, (which very few people are doing) there are still unknown variables that would need to be factored in to make the calorie equation work.

This presents a glaring problem with this equation, but it doesn’t end here. There are other, more serious problems with the calorie equation that arise because it’s predicated on several false assumptions.

Caloric Restriction, Metabolic Adaptation, and Behavioral Compensation

The first of these assumptions is that our bodies’ energy usage doesn’t change based on our environment.

There have been many times where researchers have tried to apply the calorie equation to fat loss. They set up experiments where they reduce people’s food intakes and increase their exercise, thereby reducing the number of “calories-in” and increasing the number of “calories-out.”

And these studies do result in weight loss. But the amount of weight loss is nowhere near the amount predicted by the calorie equation.

This discrepancy boils down to two main factors:

1. Metabolic Adaptation

Metabolic adaptation is how our bodies internally adjust, or adapt, to changes in caloric intake (“calories-in”) or caloric expenditure (“calories-out”). When we reduce our caloric intake or increase our caloric expenditure, our bodies reduce the amount of energy they use. And when we increase our caloric intake or decrease our caloric expenditure, our bodies increase the amount of energy they use (8, 9, 10, 11).

This is accomplished through various hormonal and enzymatic changes, which allow for adjustments in energy usage, metabolic fuel selection, and energy partitioning.

These adaptive responses throw another wrench in the calorie equation. If we factor metabolic adaptation into the equation, we would have to reduce our caloric intake even more to achieve our desired weight loss.

2. Behavioral Compensation

Behavioral compensation is how we respond externally to changes in caloric intake or expenditure. This could mean reducing the amount we exercise when we eat fewer calories or increasing the amount we eat when we exercise more.

One review that considered many weight loss studies found that, because of behavioral compensation, the amount of weight loss from caloric restriction averages to be 12-44% less than what’s predicted by the calorie equation (12). They also found the amount of weight loss from increased exercise to be 55-64% less than was expected due to behavioral compensation.

Those are HUGE differences between the mythical calorie equation and reality!

And, behavioral compensation is an even bigger factor when we increase the amount of “calories-in.” The amount of weight gain in these situations is up to 96% less than is expected from the calorie equation! (12) You read that right, 96%! That basically means that we’re really good at compensating when we eat more food than normal, to the point that it’s pretty hard to gain weight that way.

But of course, metabolic adaptation and behavioral compensation don’t mean that the mythical equation is wrong. They’re just two more variables we have to factor into the equation that at this point is unrecognizable compared to the original “calories in – calories out = change in body fat.”

Up until this point we’ve only been dealing with adjustments to the calorie equation, but after considering this next false assumption it’ll become quite clear that this equation has no place in the health or fat loss arena.

What Are Calories?

This brings us to one of the most egregious errors that underlies the calorie equation: Calories are not relevant to human physiology.

Calories are simply a measure of energy, specifically heat energy.

In the context of nutrition, we think about the number of calories, or potential energy, held in certain foods. But, we can consider the number of calories in anything, whether it’s grass, wood, or gasoline.

Now, we all know that our bodies can’t convert the energy (calories) in grass, wood, or gasoline to usable energy in our bodies. So why do we assume that we’ll equally convert the energy in all food to usable energy in our bodies?

We consider that a mango has 200 calories, a steak has 600 calories, and a doughnut has 300 calories, but we don’t consider how much of that potential energy can or will be converted to usable energy.

There are many factors that affect how much of the energy, or calories, in the food we eat will become usable energy in our bodies.

The food must first be digested and absorbed. However, the amount of the food that actually gets digested and absorbed varies greatly based on the food and our gut function, and varying amounts of energy are required for this digestion and absorption.

Once absorbed, the carbohydrates, fats, and protein from the food we eat can be used to produce energy. This occurs in the mitochondria of our cells through a process called respiration.

During this process, the food we eat is converted into a form of usable energy that’s held in a molecule called ATP. But, there are tons of factors that affect whether the carbohydrates, fats, and protein even get to the mitochondria, let alone whether they’ll be used to produce ATP.

The different macronutrients (carbs, fats, and protein) vary significantly in this regard. Carbohydrates are our primary energy source while fat is our secondary energy source. Protein, on the other hand, is not likely to be converted to usable energy through mitochondrial respiration and is instead used primarily for building and rebuilding tissues.

So, it makes little sense to equate the potential energy, or calories, between the different macronutrients, as the likelihood that they’ll be used to produce ATP varies considerably. Equating the calories between the different macronutrients actually violates the second law of thermodynamics, as is explained here:

“A review of simple thermodynamic principles shows that weight change on isocaloric diets is not expected to be independent of path (metabolism of macronutrients) and indeed such a general principle would be a violation of the second law [of thermodynamics].” “The second law of thermodynamics says that variation of efficiency for different metabolic pathways is to be expected. Thus, ironically the dictum that a “calorie is a calorie” violates the second law of thermodynamics, as a matter of principle.” (13)

And, the factors that affect mitochondrial respiration go far beyond the differences between macronutrients. They also include the hormonal state, the amount of nutrients available, the toxins present, the time of day, the ambient temperature, the amount of sunlight present, the psychological state, and virtually every other aspect of our environment.

In other words, our bodies don’t run on a calorie currency, as they must convert the energy in food that we call “calories” into energy that they can use. And the amount of calories in our food is barely relevant considering the many factors that affect its conversion to usable energy.

The problems with the misplaced focus on calories has been nicely summed up in this quote:

“It is increasingly clear that the idea that “a calorie is a calorie” is misleading… Different diets… lead to different biochemical pathways (due to the hormonal and enzymatic changes) that are not equivalent when correctly compared through the laws of thermodynamics. Unless one measures heat and the biomolecules synthesized using ATP, it is inappropriate to assume that the only thing that counts in terms of food consumption and energy balance is the intake of dietary calories and weight storage.” (6)

And, as if all of this weren’t enough, the amount of usable energy that we do produce or use doesn’t say anything about where or what that energy is used for, which is vitally important to consider for both fat loss and health!

The Dangers of Caloric Restriction

The final false assumption of the calorie equation is that any excess energy we have will become fat, while any energy deficit will result in fat loss.

This assumption that fat gain is the product of excess energy and fat loss is the product of a lack of energy is probably the single most harmful misconception that exists in the health and nutrition field.

The 1st law of thermodynamics is often cited in support of this idea, which explains that energy cannot be created or destroyed. But, this has nothing to do with where energy is used or the physiological processes of fat gain and loss.

Energy is used for virtually everything we do. It’s used to accomplish our basic daily functions, like breathing and digesting, in addition to handling stressors, like exercise and mental work. Energy is also used to maintain, repair, and grow our tissues, like muscles, bones, fascia, and organs.

All the factors we’ve mentioned so far, including our hormonal state and the many aspects of our environment, determine the partitioning of energy, or where energy is used.

For example, in the rat study that was mentioned earlier, the amount of energy from consumed protein that was allocated to fat and muscle tissue differed based on the type of protein that was consumed (4).

However, the calorie equation doesn’t acknowledge the concept of energy partitioning and instead relies on the extremely common fallacy that any excess energy we have will be used for body fat and any energy deficit will come from body fat.

While this ignores a key physiological concept, there’s another problem with this fallacy that we haven’t addressed: body fat is a storage of fuel, or potential energy. In other words, the potential energy in food is stored as body fat when it’s NOT converted to usable energy.

While this is somewhat acknowledged, it’s assumed that energy production occurs until we have enough energy, at which point any potential energy left over becomes fat. But, that couldn’t be farther from the truth.

As was mentioned earlier, energy production, or mitochondrial respiration, is affected by all sorts of variables, from the amount of nutrients available to the time of day. When energy production is inhibited based on these many factors, the potential energy from our food is stored as fat and we’re left without enough energy to properly function.

This is what underlies fat gain and the obesity epidemic. Not too much energy, but too little energy (14).

As such, the recommendations to further reduce our available energy only make the problem worse, as is explained in this quote:

“In conclusion, the presented metabolic mechanism of environmentally caused obesity indicates energy deficiency as an engine working toward development of obesity. It is obvious that all efforts to stop this engine by further decreasing the energy cannot be successful. Thus, the low calorie diets and exercise regimens seem to be a redundant burden of already exhausted people.” (14)

Unfortunately, it doesn’t end there. Our bodies adapt to energy deficiencies by further inhibiting energy production and storing more fuel as fat in order to conserve energy, resulting in a vicious cycle (10, 14, 15).

This is the biggest reason why the calorie equation is destroying our health. We already lack energy due to the inhibition of mitochondrial respiration by nutrient deficiencies and many other problems, and then we eat less and exercise more, which further reduces the amount of energy we have available to properly function, encourages fat gain, and leads to the chronic diseases we see in epidemic proportions today.

We need to put an end to this terribly misguided approach to fat loss and health and instead shift our focus to the process of energy production. By increasing the amount of energy we produce, we can reduce the storage of food as body fat which will allow us to lose fat while also improving our health.

As I’m sure you’ve already gathered, there are quite a few factors affecting energy production. If you want to learn more about those factors and learn to lose fat the healthy way, sign up for the free mini-course below!

References

The Mythical Calorie Equation

Calories In – Calorie Out = Change in Body Fat

This ubiquitous equation represents the idea that the difference between the number of calories we consume and the number of calories we expend determines the amount of fat we gain or lose. It’s a wonderfully simple conception, although not an accurate one, and actually a very dangerous one.

It’s truly amazing to me that this equation has stuck around this long. The entire concept is illogical to begin with, not to mention the mounds of evidence against it.

Yet, the dogmatic adherence to this equation has informed so much of the current nutrition recommendations. This is especially true when it comes to fat loss, where “eat less and exercise more” is the common mantra. But it has also been applied to the general health recommendations to eat foods that are less calorie-dense, drink more water, and consume more protein and fiber to keep us full for longer, among many others.

While the fact that we associate calories with fat gain and loss is bad, the fact that we associate them with health is even worse.

But before we dive in too far, let’s start by exploring the extensive evidence that refutes the validity of equation.

Isocaloric Studies

If the calorie equation was valid, then consuming diets containing different foods with the same number of calories would have the same effects on body fat. But, many studies that have tested this hypothesis have shown that this isn’t the case. Let’s take a look at a few of them.

This first study, performed in a metabolic ward, had subjects on isocaloric reduced-fat or reduced-carbohydrate diets (1) (isocaloric means the diets had the same number of calories). They found that subjects on the reduced-fat diets lost more body fat than subjects on the reduced-carb diets. And, those on the reduced-fat diets lost less weight than those on the reduced-carb diets, meaning that a much higher percentage of the weight they lost was fat.

[This study also provides more evidence against the “burn fat for fat loss” fallacy, as those on the reduced-carb diets burned more fat than the reduced-fat group even though they lost less body fat.]

This next study also compared subjects on isocaloric diets with varying amounts of carbs and fat, although this one was performed on rats instead of humans (2). They found that the rats on the high-fat diets had higher total body fat by the end of the study than those on the control diet, but those on the high-carb diets didn’t. Again, remember that the high-fat and high-carb rats were fed the exact same number of calories!

In this study, human subjects were given 1 of 3 isocaloric diets that contained varying amounts of carbohydrates, and they found huge differences in weight loss, fat loss, and percent weight loss based on the amount of carbohydrates in the diet (3). In fact, those on the diet that was highest in carbohydrates lost 14 pounds more of body fat than those on the lowest carbohydrate diet during the 9-week intervention! In reference to these results, the authors commented that “no adequate explanation [could] be given for [the] weight loss differences.”

There are many more isocaloric studies that provide similar evidence against the calorie equation, including one on rats where two groups were fed the exact same diet except for the type of protein and ended up with a 26% difference in fat mass (4) and other studies showing that changing the amount of fat or carbohydrate in the diet affected the amount of body fat gained or lost, even when consuming the same number of calories (5, 6).

It’s clear based on these studies that the calorie equation isn’t quite as simple as it was made out to be. The types of foods that are eaten have a substantial effect on changes in body fat, rather than simply the number of “calories-in.”

Now, the argument can be made that changing the types of foods simply changes the number of “calories-out.” And, while this is true, it’s often entirely ignored in favor of the recommendations to simply “eat less and exercise more.”

Even when not ignored, the fact that the type of food, rather than simply the number of calories, affects the number of “calories-out” creates problems of its own.

It’s known that different diet compositions can vary in their metabolizable energy (the amount of energy in the food that’s actually digested and absorbed) and thermic effects (the amount of energy required for digesting and using the food). It’s also acknowledged that different diet compositions can cause changes in the resting metabolic rate and physical activity levels. But, some of the effects of different diet compositions can’t be fully explained yet.

This review, aimed at figuring out whether we can account for all the energetic effects of different diet compositions, looked at many calorie-controlled weight loss studies (7). They found that “neither macronutrient-specific differences in the availability of dietary energy nor changes in energy expenditure could explain [the] differences in weight loss” and concluded by suggesting that “further research is needed to identify the mechanisms that result in greater weight loss with one diet than with another.”

In other words, even if we account for differences in metabolizable energy, thermic effects, resting metabolic rate, and physical activity levels, (which very few people are doing) there are still unknown variables that would need to be factored in to make the calorie equation work.

This presents a glaring problem with this equation, but it doesn’t end here. There are other, more serious problems with the calorie equation that arise because it’s predicated on several false assumptions.

Caloric Restriction, Metabolic Adaptation, and Behavioral Compensation

The first of these assumptions is that our bodies’ energy usage doesn’t change based on our environment.

There have been many times where researchers have tried to apply the calorie equation to fat loss. They set up experiments where they reduce people’s food intakes and increase their exercise, thereby reducing the number of “calories-in” and increasing the number of “calories-out.”

And these studies do result in weight loss. But the amount of weight loss is nowhere near the amount predicted by the calorie equation.

This discrepancy boils down to two main factors:

1. Metabolic Adaptation

Metabolic adaptation is how our bodies internally adjust, or adapt, to changes in caloric intake (“calories-in”) or caloric expenditure (“calories-out”). When we reduce our caloric intake or increase our caloric expenditure, our bodies reduce the amount of energy they use. And when we increase our caloric intake or decrease our caloric expenditure, our bodies increase the amount of energy they use (8, 9, 10, 11).

This is accomplished through various hormonal and enzymatic changes, which allow for adjustments in energy usage, metabolic fuel selection, and energy partitioning.

These adaptive responses throw another wrench in the calorie equation. If we factor metabolic adaptation into the equation, we would have to reduce our caloric intake even more to achieve our desired weight loss.

2. Behavioral Compensation

Behavioral compensation is how we respond externally to changes in caloric intake or expenditure. This could mean reducing the amount we exercise when we eat fewer calories or increasing the amount we eat when we exercise more.

One review that considered many weight loss studies found that, because of behavioral compensation, the amount of weight loss from caloric restriction averages to be 12-44% less than what’s predicted by the calorie equation (12). They also found the amount of weight loss from increased exercise to be 55-64% less than was expected due to behavioral compensation.

Those are HUGE differences between the mythical calorie equation and reality!

And, behavioral compensation is an even bigger factor when we increase the amount of “calories-in.” The amount of weight gain in these situations is up to 96% less than is expected from the calorie equation! (12) You read that right, 96%! That basically means that we’re really good at compensating when we eat more food than normal, to the point that it’s pretty hard to gain weight that way.

But of course, metabolic adaptation and behavioral compensation don’t mean that the mythical equation is wrong. They’re just two more variables we have to factor into the equation that at this point is unrecognizable compared to the original “calories in – calories out = change in body fat.”

Up until this point we’ve only been dealing with adjustments to the calorie equation, but after considering this next false assumption it’ll become quite clear that this equation has no place in the health or fat loss arena.

What Are Calories?

This brings us to one of the most egregious errors that underlies the calorie equation: Calories are not relevant to human physiology.

Calories are simply a measure of energy, specifically heat energy.

In the context of nutrition, we think about the number of calories, or potential energy, held in certain foods. But, we can consider the number of calories in anything, whether it’s grass, wood, or gasoline.

Now, we all know that our bodies can’t convert the energy (calories) in grass, wood, or gasoline to usable energy in our bodies. So why do we assume that we’ll equally convert the energy in all food to usable energy in our bodies?

We consider that a mango has 200 calories, a steak has 600 calories, and a doughnut has 300 calories, but we don’t consider how much of that potential energy can or will be converted to usable energy.

There are many factors that affect how much of the energy, or calories, in the food we eat will become usable energy in our bodies.

The food must first be digested and absorbed. However, the amount of the food that actually gets digested and absorbed varies greatly based on the food and our gut function, and varying amounts of energy are required for this digestion and absorption.

Once absorbed, the carbohydrates, fats, and protein from the food we eat can be used to produce energy. This occurs in the mitochondria of our cells through a process called respiration.

During this process, the food we eat is converted into a form of usable energy that’s held in a molecule called ATP. But, there are tons of factors that affect whether the carbohydrates, fats, and protein even get to the mitochondria, let alone whether they’ll be used to produce ATP.

The different macronutrients (carbs, fats, and protein) vary significantly in this regard. Carbohydrates are our primary energy source while fat is our secondary energy source. Protein, on the other hand, is not likely to be converted to usable energy through mitochondrial respiration and is instead used primarily for building and rebuilding tissues.

So, it makes little sense to equate the potential energy, or calories, between the different macronutrients, as the likelihood that they’ll be used to produce ATP varies considerably. Equating the calories between the different macronutrients actually violates the second law of thermodynamics, as is explained here:

“A review of simple thermodynamic principles shows that weight change on isocaloric diets is not expected to be independent of path (metabolism of macronutrients) and indeed such a general principle would be a violation of the second law [of thermodynamics].” “The second law of thermodynamics says that variation of efficiency for different metabolic pathways is to be expected. Thus, ironically the dictum that a “calorie is a calorie” violates the second law of thermodynamics, as a matter of principle.” (13)

And, the factors that affect mitochondrial respiration go far beyond the differences between macronutrients. They also include the hormonal state, the amount of nutrients available, the toxins present, the time of day, the ambient temperature, the amount of sunlight present, the psychological state, and virtually every other aspect of our environment.

In other words, our bodies don’t run on a calorie currency, as they must convert the energy in food that we call “calories” into energy that they can use. And the amount of calories in our food is barely relevant considering the many factors that affect its conversion to usable energy.

The problems with the misplaced focus on calories has been nicely summed up in this quote:

“It is increasingly clear that the idea that “a calorie is a calorie” is misleading… Different diets… lead to different biochemical pathways (due to the hormonal and enzymatic changes) that are not equivalent when correctly compared through the laws of thermodynamics. Unless one measures heat and the biomolecules synthesized using ATP, it is inappropriate to assume that the only thing that counts in terms of food consumption and energy balance is the intake of dietary calories and weight storage.” (6)

And, as if all of this weren’t enough, the amount of usable energy that we do produce or use doesn’t say anything about where or what that energy is used for, which is vitally important to consider for both fat loss and health!

The Dangers of Caloric Restriction

The final false assumption of the calorie equation is that any excess energy we have will become fat, while any energy deficit will result in fat loss.

This assumption that fat gain is the product of excess energy and fat loss is the product of a lack of energy is probably the single most harmful misconception that exists in the health and nutrition field.

The 1st law of thermodynamics is often cited in support of this idea, which explains that energy cannot be created or destroyed. But, this has nothing to do with where energy is used or the physiological processes of fat gain and loss.

Energy is used for virtually everything we do. It’s used to accomplish our basic daily functions, like breathing and digesting, in addition to handling stressors, like exercise and mental work. Energy is also used to maintain, repair, and grow our tissues, like muscles, bones, fascia, and organs.

All the factors we’ve mentioned so far, including our hormonal state and the many aspects of our environment, determine the partitioning of energy, or where energy is used.

For example, in the rat study that was mentioned earlier, the amount of energy from consumed protein that was allocated to fat and muscle tissue differed based on the type of protein that was consumed (4).

However, the calorie equation doesn’t acknowledge the concept of energy partitioning and instead relies on the extremely common fallacy that any excess energy we have will be used for body fat and any energy deficit will come from body fat.

While this ignores a key physiological concept, there’s another problem with this fallacy that we haven’t addressed: body fat is a storage of fuel, or potential energy. In other words, the potential energy in food is stored as body fat when it’s NOT converted to usable energy.

While this is somewhat acknowledged, it’s assumed that energy production occurs until we have enough energy, at which point any potential energy left over becomes fat. But, that couldn’t be farther from the truth.

As was mentioned earlier, energy production, or mitochondrial respiration, is affected by all sorts of variables, from the amount of nutrients available to the time of day. When energy production is inhibited based on these many factors, the potential energy from our food is stored as fat and we’re left without enough energy to properly function.

This is what underlies fat gain and the obesity epidemic. Not too much energy, but too little energy (14).

As such, the recommendations to further reduce our available energy only make the problem worse, as is explained in this quote:

“In conclusion, the presented metabolic mechanism of environmentally caused obesity indicates energy deficiency as an engine working toward development of obesity. It is obvious that all efforts to stop this engine by further decreasing the energy cannot be successful. Thus, the low calorie diets and exercise regimens seem to be a redundant burden of already exhausted people.” (14)

Unfortunately, it doesn’t end there. Our bodies adapt to energy deficiencies by further inhibiting energy production and storing more fuel as fat in order to conserve energy, resulting in a vicious cycle (10, 14, 15).

This is the biggest reason why the calorie equation is destroying our health. We already lack energy due to the inhibition of mitochondrial respiration by nutrient deficiencies and many other problems, and then we eat less and exercise more, which further reduces the amount of energy we have available to properly function, encourages fat gain, and leads to the chronic diseases we see in epidemic proportions today.

We need to put an end to this terribly misguided approach to fat loss and health and instead shift our focus to the process of energy production. By increasing the amount of energy we produce, we can reduce the storage of food as body fat which will allow us to lose fat while also improving our health.

As I’m sure you’ve already gathered, there are quite a few factors affecting energy production. If you want to learn more about those factors and learn to lose fat the healthy way, sign up for the free mini-course below!

References

The Mythical Calorie Equation

Calories In – Calorie Out = Change in Body Fat

This ubiquitous equation represents the idea that the difference between the number of calories we consume and the number of calories we expend determines the amount of fat we gain or lose. It’s a wonderfully simple conception, although not an accurate one, and actually a very dangerous one.

It’s truly amazing to me that this equation has stuck around this long. The entire concept is illogical to begin with, not to mention the mounds of evidence against it.

Yet, the dogmatic adherence to this equation has informed so much of the current nutrition recommendations. This is especially true when it comes to fat loss, where “eat less and exercise more” is the common mantra. But it has also been applied to the general health recommendations to eat foods that are less calorie-dense, drink more water, and consume more protein and fiber to keep us full for longer, among many others.

While the fact that we associate calories with fat gain and loss is bad, the fact that we associate them with health is even worse.

But before we dive in too far, let’s start by exploring the extensive evidence that refutes the validity of equation.

Isocaloric Studies

If the calorie equation was valid, then consuming diets containing different foods with the same number of calories would have the same effects on body fat. But, many studies that have tested this hypothesis have shown that this isn’t the case. Let’s take a look at a few of them.

This first study, performed in a metabolic ward, had subjects on isocaloric reduced-fat or reduced-carbohydrate diets (1) (isocaloric means the diets had the same number of calories). They found that subjects on the reduced-fat diets lost more body fat than subjects on the reduced-carb diets. And, those on the reduced-fat diets lost less weight than those on the reduced-carb diets, meaning that a much higher percentage of the weight they lost was fat.

[This study also provides more evidence against the “burn fat for fat loss” fallacy, as those on the reduced-carb diets burned more fat than the reduced-fat group even though they lost less body fat.]

This next study also compared subjects on isocaloric diets with varying amounts of carbs and fat, although this one was performed on rats instead of humans (2). They found that the rats on the high-fat diets had higher total body fat by the end of the study than those on the control diet, but those on the high-carb diets didn’t. Again, remember that the high-fat and high-carb rats were fed the exact same number of calories!

In this study, human subjects were given 1 of 3 isocaloric diets that contained varying amounts of carbohydrates, and they found huge differences in weight loss, fat loss, and percent weight loss based on the amount of carbohydrates in the diet (3). In fact, those on the diet that was highest in carbohydrates lost 14 pounds more of body fat than those on the lowest carbohydrate diet during the 9-week intervention! In reference to these results, the authors commented that “no adequate explanation [could] be given for [the] weight loss differences.”

There are many more isocaloric studies that provide similar evidence against the calorie equation, including one on rats where two groups were fed the exact same diet except for the type of protein and ended up with a 26% difference in fat mass (4) and other studies showing that changing the amount of fat or carbohydrate in the diet affected the amount of body fat gained or lost, even when consuming the same number of calories (5, 6).

It’s clear based on these studies that the calorie equation isn’t quite as simple as it was made out to be. The types of foods that are eaten have a substantial effect on changes in body fat, rather than simply the number of “calories-in.”

Now, the argument can be made that changing the types of foods simply changes the number of “calories-out.” And, while this is true, it’s often entirely ignored in favor of the recommendations to simply “eat less and exercise more.”

Even when not ignored, the fact that the type of food, rather than simply the number of calories, affects the number of “calories-out” creates problems of its own.

It’s known that different diet compositions can vary in their metabolizable energy (the amount of energy in the food that’s actually digested and absorbed) and thermic effects (the amount of energy required for digesting and using the food). It’s also acknowledged that different diet compositions can cause changes in the resting metabolic rate and physical activity levels. But, some of the effects of different diet compositions can’t be fully explained yet.

This review, aimed at figuring out whether we can account for all the energetic effects of different diet compositions, looked at many calorie-controlled weight loss studies (7). They found that “neither macronutrient-specific differences in the availability of dietary energy nor changes in energy expenditure could explain [the] differences in weight loss” and concluded by suggesting that “further research is needed to identify the mechanisms that result in greater weight loss with one diet than with another.”

In other words, even if we account for differences in metabolizable energy, thermic effects, resting metabolic rate, and physical activity levels, (which very few people are doing) there are still unknown variables that would need to be factored in to make the calorie equation work.

This presents a glaring problem with this equation, but it doesn’t end here. There are other, more serious problems with the calorie equation that arise because it’s predicated on several false assumptions.

Caloric Restriction, Metabolic Adaptation, and Behavioral Compensation

The first of these assumptions is that our bodies’ energy usage doesn’t change based on our environment.

There have been many times where researchers have tried to apply the calorie equation to fat loss. They set up experiments where they reduce people’s food intakes and increase their exercise, thereby reducing the number of “calories-in” and increasing the number of “calories-out.”

And these studies do result in weight loss. But the amount of weight loss is nowhere near the amount predicted by the calorie equation.

This discrepancy boils down to two main factors:

1. Metabolic Adaptation

Metabolic adaptation is how our bodies internally adjust, or adapt, to changes in caloric intake (“calories-in”) or caloric expenditure (“calories-out”). When we reduce our caloric intake or increase our caloric expenditure, our bodies reduce the amount of energy they use. And when we increase our caloric intake or decrease our caloric expenditure, our bodies increase the amount of energy they use (8, 9, 10, 11).

This is accomplished through various hormonal and enzymatic changes, which allow for adjustments in energy usage, metabolic fuel selection, and energy partitioning.

These adaptive responses throw another wrench in the calorie equation. If we factor metabolic adaptation into the equation, we would have to reduce our caloric intake even more to achieve our desired weight loss.

2. Behavioral Compensation

Behavioral compensation is how we respond externally to changes in caloric intake or expenditure. This could mean reducing the amount we exercise when we eat fewer calories or increasing the amount we eat when we exercise more.

One review that considered many weight loss studies found that, because of behavioral compensation, the amount of weight loss from caloric restriction averages to be 12-44% less than what’s predicted by the calorie equation (12). They also found the amount of weight loss from increased exercise to be 55-64% less than was expected due to behavioral compensation.

Those are HUGE differences between the mythical calorie equation and reality!

And, behavioral compensation is an even bigger factor when we increase the amount of “calories-in.” The amount of weight gain in these situations is up to 96% less than is expected from the calorie equation! (12) You read that right, 96%! That basically means that we’re really good at compensating when we eat more food than normal, to the point that it’s pretty hard to gain weight that way.

But of course, metabolic adaptation and behavioral compensation don’t mean that the mythical equation is wrong. They’re just two more variables we have to factor into the equation that at this point is unrecognizable compared to the original “calories in – calories out = change in body fat.”

Up until this point we’ve only been dealing with adjustments to the calorie equation, but after considering this next false assumption it’ll become quite clear that this equation has no place in the health or fat loss arena.

What Are Calories?

This brings us to one of the most egregious errors that underlies the calorie equation: Calories are not relevant to human physiology.

Calories are simply a measure of energy, specifically heat energy.

In the context of nutrition, we think about the number of calories, or potential energy, held in certain foods. But, we can consider the number of calories in anything, whether it’s grass, wood, or gasoline.

Now, we all know that our bodies can’t convert the energy (calories) in grass, wood, or gasoline to usable energy in our bodies. So why do we assume that we’ll equally convert the energy in all food to usable energy in our bodies?

We consider that a mango has 200 calories, a steak has 600 calories, and a doughnut has 300 calories, but we don’t consider how much of that potential energy can or will be converted to usable energy.

There are many factors that affect how much of the energy, or calories, in the food we eat will become usable energy in our bodies.

The food must first be digested and absorbed. However, the amount of the food that actually gets digested and absorbed varies greatly based on the food and our gut function, and varying amounts of energy are required for this digestion and absorption.

Once absorbed, the carbohydrates, fats, and protein from the food we eat can be used to produce energy. This occurs in the mitochondria of our cells through a process called respiration.

During this process, the food we eat is converted into a form of usable energy that’s held in a molecule called ATP. But, there are tons of factors that affect whether the carbohydrates, fats, and protein even get to the mitochondria, let alone whether they’ll be used to produce ATP.

The different macronutrients (carbs, fats, and protein) vary significantly in this regard. Carbohydrates are our primary energy source while fat is our secondary energy source. Protein, on the other hand, is not likely to be converted to usable energy through mitochondrial respiration and is instead used primarily for building and rebuilding tissues.

So, it makes little sense to equate the potential energy, or calories, between the different macronutrients, as the likelihood that they’ll be used to produce ATP varies considerably. Equating the calories between the different macronutrients actually violates the second law of thermodynamics, as is explained here:

“A review of simple thermodynamic principles shows that weight change on isocaloric diets is not expected to be independent of path (metabolism of macronutrients) and indeed such a general principle would be a violation of the second law [of thermodynamics].” “The second law of thermodynamics says that variation of efficiency for different metabolic pathways is to be expected. Thus, ironically the dictum that a “calorie is a calorie” violates the second law of thermodynamics, as a matter of principle.” (13)

And, the factors that affect mitochondrial respiration go far beyond the differences between macronutrients. They also include the hormonal state, the amount of nutrients available, the toxins present, the time of day, the ambient temperature, the amount of sunlight present, the psychological state, and virtually every other aspect of our environment.

In other words, our bodies don’t run on a calorie currency, as they must convert the energy in food that we call “calories” into energy that they can use. And the amount of calories in our food is barely relevant considering the many factors that affect its conversion to usable energy.

The problems with the misplaced focus on calories has been nicely summed up in this quote:

“It is increasingly clear that the idea that “a calorie is a calorie” is misleading… Different diets… lead to different biochemical pathways (due to the hormonal and enzymatic changes) that are not equivalent when correctly compared through the laws of thermodynamics. Unless one measures heat and the biomolecules synthesized using ATP, it is inappropriate to assume that the only thing that counts in terms of food consumption and energy balance is the intake of dietary calories and weight storage.” (6)

And, as if all of this weren’t enough, the amount of usable energy that we do produce or use doesn’t say anything about where or what that energy is used for, which is vitally important to consider for both fat loss and health!

The Dangers of Caloric Restriction

The final false assumption of the calorie equation is that any excess energy we have will become fat, while any energy deficit will result in fat loss.

This assumption that fat gain is the product of excess energy and fat loss is the product of a lack of energy is probably the single most harmful misconception that exists in the health and nutrition field.

The 1st law of thermodynamics is often cited in support of this idea, which explains that energy cannot be created or destroyed. But, this has nothing to do with where energy is used or the physiological processes of fat gain and loss.

Energy is used for virtually everything we do. It’s used to accomplish our basic daily functions, like breathing and digesting, in addition to handling stressors, like exercise and mental work. Energy is also used to maintain, repair, and grow our tissues, like muscles, bones, fascia, and organs.

All the factors we’ve mentioned so far, including our hormonal state and the many aspects of our environment, determine the partitioning of energy, or where energy is used.

For example, in the rat study that was mentioned earlier, the amount of energy from consumed protein that was allocated to fat and muscle tissue differed based on the type of protein that was consumed (4).

However, the calorie equation doesn’t acknowledge the concept of energy partitioning and instead relies on the extremely common fallacy that any excess energy we have will be used for body fat and any energy deficit will come from body fat.

While this ignores a key physiological concept, there’s another problem with this fallacy that we haven’t addressed: body fat is a storage of fuel, or potential energy. In other words, the potential energy in food is stored as body fat when it’s NOT converted to usable energy.

While this is somewhat acknowledged, it’s assumed that energy production occurs until we have enough energy, at which point any potential energy left over becomes fat. But, that couldn’t be farther from the truth.

As was mentioned earlier, energy production, or mitochondrial respiration, is affected by all sorts of variables, from the amount of nutrients available to the time of day. When energy production is inhibited based on these many factors, the potential energy from our food is stored as fat and we’re left without enough energy to properly function.

This is what underlies fat gain and the obesity epidemic. Not too much energy, but too little energy (14).

As such, the recommendations to further reduce our available energy only make the problem worse, as is explained in this quote:

“In conclusion, the presented metabolic mechanism of environmentally caused obesity indicates energy deficiency as an engine working toward development of obesity. It is obvious that all efforts to stop this engine by further decreasing the energy cannot be successful. Thus, the low calorie diets and exercise regimens seem to be a redundant burden of already exhausted people.” (14)

Unfortunately, it doesn’t end there. Our bodies adapt to energy deficiencies by further inhibiting energy production and storing more fuel as fat in order to conserve energy, resulting in a vicious cycle (10, 14, 15).

This is the biggest reason why the calorie equation is destroying our health. We already lack energy due to the inhibition of mitochondrial respiration by nutrient deficiencies and many other problems, and then we eat less and exercise more, which further reduces the amount of energy we have available to properly function, encourages fat gain, and leads to the chronic diseases we see in epidemic proportions today.

We need to put an end to this terribly misguided approach to fat loss and health and instead shift our focus to the process of energy production. By increasing the amount of energy we produce, we can reduce the storage of food as body fat which will allow us to lose fat while also improving our health.

As I’m sure you’ve already gathered, there are quite a few factors affecting energy production. If you want to learn more about those factors and learn to lose fat the healthy way, sign up for the free mini-course below!

References

The Mythical Calorie Equation

Calories In – Calorie Out = Change in Body Fat

This ubiquitous equation represents the idea that the difference between the number of calories we consume and the number of calories we expend determines the amount of fat we gain or lose. It’s a wonderfully simple conception, although not an accurate one, and actually a very dangerous one.

It’s truly amazing to me that this equation has stuck around this long. The entire concept is illogical to begin with, not to mention the mounds of evidence against it.

Yet, the dogmatic adherence to this equation has informed so much of the current nutrition recommendations. This is especially true when it comes to fat loss, where “eat less and exercise more” is the common mantra. But it has also been applied to the general health recommendations to eat foods that are less calorie-dense, drink more water, and consume more protein and fiber to keep us full for longer, among many others.

While the fact that we associate calories with fat gain and loss is bad, the fact that we associate them with health is even worse.

But before we dive in too far, let’s start by exploring the extensive evidence that refutes the validity of equation.

Isocaloric Studies

If the calorie equation was valid, then consuming diets containing different foods with the same number of calories would have the same effects on body fat. But, many studies that have tested this hypothesis have shown that this isn’t the case. Let’s take a look at a few of them.

This first study, performed in a metabolic ward, had subjects on isocaloric reduced-fat or reduced-carbohydrate diets (1) (isocaloric means the diets had the same number of calories). They found that subjects on the reduced-fat diets lost more body fat than subjects on the reduced-carb diets. And, those on the reduced-fat diets lost less weight than those on the reduced-carb diets, meaning that a much higher percentage of the weight they lost was fat.

[This study also provides more evidence against the “burn fat for fat loss” fallacy, as those on the reduced-carb diets burned more fat than the reduced-fat group even though they lost less body fat.]

This next study also compared subjects on isocaloric diets with varying amounts of carbs and fat, although this one was performed on rats instead of humans (2). They found that the rats on the high-fat diets had higher total body fat by the end of the study than those on the control diet, but those on the high-carb diets didn’t. Again, remember that the high-fat and high-carb rats were fed the exact same number of calories!

In this study, human subjects were given 1 of 3 isocaloric diets that contained varying amounts of carbohydrates, and they found huge differences in weight loss, fat loss, and percent weight loss based on the amount of carbohydrates in the diet (3). In fact, those on the diet that was highest in carbohydrates lost 14 pounds more of body fat than those on the lowest carbohydrate diet during the 9-week intervention! In reference to these results, the authors commented that “no adequate explanation [could] be given for [the] weight loss differences.”

There are many more isocaloric studies that provide similar evidence against the calorie equation, including one on rats where two groups were fed the exact same diet except for the type of protein and ended up with a 26% difference in fat mass (4) and other studies showing that changing the amount of fat or carbohydrate in the diet affected the amount of body fat gained or lost, even when consuming the same number of calories (5, 6).

It’s clear based on these studies that the calorie equation isn’t quite as simple as it was made out to be. The types of foods that are eaten have a substantial effect on changes in body fat, rather than simply the number of “calories-in.”

Now, the argument can be made that changing the types of foods simply changes the number of “calories-out.” And, while this is true, it’s often entirely ignored in favor of the recommendations to simply “eat less and exercise more.”

Even when not ignored, the fact that the type of food, rather than simply the number of calories, affects the number of “calories-out” creates problems of its own.

It’s known that different diet compositions can vary in their metabolizable energy (the amount of energy in the food that’s actually digested and absorbed) and thermic effects (the amount of energy required for digesting and using the food). It’s also acknowledged that different diet compositions can cause changes in the resting metabolic rate and physical activity levels. But, some of the effects of different diet compositions can’t be fully explained yet.

This review, aimed at figuring out whether we can account for all the energetic effects of different diet compositions, looked at many calorie-controlled weight loss studies (7). They found that “neither macronutrient-specific differences in the availability of dietary energy nor changes in energy expenditure could explain [the] differences in weight loss” and concluded by suggesting that “further research is needed to identify the mechanisms that result in greater weight loss with one diet than with another.”

In other words, even if we account for differences in metabolizable energy, thermic effects, resting metabolic rate, and physical activity levels, (which very few people are doing) there are still unknown variables that would need to be factored in to make the calorie equation work.

This presents a glaring problem with this equation, but it doesn’t end here. There are other, more serious problems with the calorie equation that arise because it’s predicated on several false assumptions.

Caloric Restriction, Metabolic Adaptation, and Behavioral Compensation

The first of these assumptions is that our bodies’ energy usage doesn’t change based on our environment.

There have been many times where researchers have tried to apply the calorie equation to fat loss. They set up experiments where they reduce people’s food intakes and increase their exercise, thereby reducing the number of “calories-in” and increasing the number of “calories-out.”

And these studies do result in weight loss. But the amount of weight loss is nowhere near the amount predicted by the calorie equation.

This discrepancy boils down to two main factors:

1. Metabolic Adaptation

Metabolic adaptation is how our bodies internally adjust, or adapt, to changes in caloric intake (“calories-in”) or caloric expenditure (“calories-out”). When we reduce our caloric intake or increase our caloric expenditure, our bodies reduce the amount of energy they use. And when we increase our caloric intake or decrease our caloric expenditure, our bodies increase the amount of energy they use (8, 9, 10, 11).

This is accomplished through various hormonal and enzymatic changes, which allow for adjustments in energy usage, metabolic fuel selection, and energy partitioning.

These adaptive responses throw another wrench in the calorie equation. If we factor metabolic adaptation into the equation, we would have to reduce our caloric intake even more to achieve our desired weight loss.

2. Behavioral Compensation

Behavioral compensation is how we respond externally to changes in caloric intake or expenditure. This could mean reducing the amount we exercise when we eat fewer calories or increasing the amount we eat when we exercise more.

One review that considered many weight loss studies found that, because of behavioral compensation, the amount of weight loss from caloric restriction averages to be 12-44% less than what’s predicted by the calorie equation (12). They also found the amount of weight loss from increased exercise to be 55-64% less than was expected due to behavioral compensation.

Those are HUGE differences between the mythical calorie equation and reality!

And, behavioral compensation is an even bigger factor when we increase the amount of “calories-in.” The amount of weight gain in these situations is up to 96% less than is expected from the calorie equation! (12) You read that right, 96%! That basically means that we’re really good at compensating when we eat more food than normal, to the point that it’s pretty hard to gain weight that way.

But of course, metabolic adaptation and behavioral compensation don’t mean that the mythical equation is wrong. They’re just two more variables we have to factor into the equation that at this point is unrecognizable compared to the original “calories in – calories out = change in body fat.”

Up until this point we’ve only been dealing with adjustments to the calorie equation, but after considering this next false assumption it’ll become quite clear that this equation has no place in the health or fat loss arena.

What Are Calories?

This brings us to one of the most egregious errors that underlies the calorie equation: Calories are not relevant to human physiology.

Calories are simply a measure of energy, specifically heat energy.

In the context of nutrition, we think about the number of calories, or potential energy, held in certain foods. But, we can consider the number of calories in anything, whether it’s grass, wood, or gasoline.

Now, we all know that our bodies can’t convert the energy (calories) in grass, wood, or gasoline to usable energy in our bodies. So why do we assume that we’ll equally convert the energy in all food to usable energy in our bodies?

We consider that a mango has 200 calories, a steak has 600 calories, and a doughnut has 300 calories, but we don’t consider how much of that potential energy can or will be converted to usable energy.

There are many factors that affect how much of the energy, or calories, in the food we eat will become usable energy in our bodies.

The food must first be digested and absorbed. However, the amount of the food that actually gets digested and absorbed varies greatly based on the food and our gut function, and varying amounts of energy are required for this digestion and absorption.

Once absorbed, the carbohydrates, fats, and protein from the food we eat can be used to produce energy. This occurs in the mitochondria of our cells through a process called respiration.

During this process, the food we eat is converted into a form of usable energy that’s held in a molecule called ATP. But, there are tons of factors that affect whether the carbohydrates, fats, and protein even get to the mitochondria, let alone whether they’ll be used to produce ATP.

The different macronutrients (carbs, fats, and protein) vary significantly in this regard. Carbohydrates are our primary energy source while fat is our secondary energy source. Protein, on the other hand, is not likely to be converted to usable energy through mitochondrial respiration and is instead used primarily for building and rebuilding tissues.

So, it makes little sense to equate the potential energy, or calories, between the different macronutrients, as the likelihood that they’ll be used to produce ATP varies considerably. Equating the calories between the different macronutrients actually violates the second law of thermodynamics, as is explained here:

“A review of simple thermodynamic principles shows that weight change on isocaloric diets is not expected to be independent of path (metabolism of macronutrients) and indeed such a general principle would be a violation of the second law [of thermodynamics].” “The second law of thermodynamics says that variation of efficiency for different metabolic pathways is to be expected. Thus, ironically the dictum that a “calorie is a calorie” violates the second law of thermodynamics, as a matter of principle.” (13)

And, the factors that affect mitochondrial respiration go far beyond the differences between macronutrients. They also include the hormonal state, the amount of nutrients available, the toxins present, the time of day, the ambient temperature, the amount of sunlight present, the psychological state, and virtually every other aspect of our environment.

In other words, our bodies don’t run on a calorie currency, as they must convert the energy in food that we call “calories” into energy that they can use. And the amount of calories in our food is barely relevant considering the many factors that affect its conversion to usable energy.

The problems with the misplaced focus on calories has been nicely summed up in this quote:

“It is increasingly clear that the idea that “a calorie is a calorie” is misleading… Different diets… lead to different biochemical pathways (due to the hormonal and enzymatic changes) that are not equivalent when correctly compared through the laws of thermodynamics. Unless one measures heat and the biomolecules synthesized using ATP, it is inappropriate to assume that the only thing that counts in terms of food consumption and energy balance is the intake of dietary calories and weight storage.” (6)

And, as if all of this weren’t enough, the amount of usable energy that we do produce or use doesn’t say anything about where or what that energy is used for, which is vitally important to consider for both fat loss and health!

The Dangers of Caloric Restriction

The final false assumption of the calorie equation is that any excess energy we have will become fat, while any energy deficit will result in fat loss.

This assumption that fat gain is the product of excess energy and fat loss is the product of a lack of energy is probably the single most harmful misconception that exists in the health and nutrition field.

The 1st law of thermodynamics is often cited in support of this idea, which explains that energy cannot be created or destroyed. But, this has nothing to do with where energy is used or the physiological processes of fat gain and loss.

Energy is used for virtually everything we do. It’s used to accomplish our basic daily functions, like breathing and digesting, in addition to handling stressors, like exercise and mental work. Energy is also used to maintain, repair, and grow our tissues, like muscles, bones, fascia, and organs.

All the factors we’ve mentioned so far, including our hormonal state and the many aspects of our environment, determine the partitioning of energy, or where energy is used.

For example, in the rat study that was mentioned earlier, the amount of energy from consumed protein that was allocated to fat and muscle tissue differed based on the type of protein that was consumed (4).

However, the calorie equation doesn’t acknowledge the concept of energy partitioning and instead relies on the extremely common fallacy that any excess energy we have will be used for body fat and any energy deficit will come from body fat.

While this ignores a key physiological concept, there’s another problem with this fallacy that we haven’t addressed: body fat is a storage of fuel, or potential energy. In other words, the potential energy in food is stored as body fat when it’s NOT converted to usable energy.

While this is somewhat acknowledged, it’s assumed that energy production occurs until we have enough energy, at which point any potential energy left over becomes fat. But, that couldn’t be farther from the truth.

As was mentioned earlier, energy production, or mitochondrial respiration, is affected by all sorts of variables, from the amount of nutrients available to the time of day. When energy production is inhibited based on these many factors, the potential energy from our food is stored as fat and we’re left without enough energy to properly function.

This is what underlies fat gain and the obesity epidemic. Not too much energy, but too little energy (14).

As such, the recommendations to further reduce our available energy only make the problem worse, as is explained in this quote:

“In conclusion, the presented metabolic mechanism of environmentally caused obesity indicates energy deficiency as an engine working toward development of obesity. It is obvious that all efforts to stop this engine by further decreasing the energy cannot be successful. Thus, the low calorie diets and exercise regimens seem to be a redundant burden of already exhausted people.” (14)

Unfortunately, it doesn’t end there. Our bodies adapt to energy deficiencies by further inhibiting energy production and storing more fuel as fat in order to conserve energy, resulting in a vicious cycle (10, 14, 15).

This is the biggest reason why the calorie equation is destroying our health. We already lack energy due to the inhibition of mitochondrial respiration by nutrient deficiencies and many other problems, and then we eat less and exercise more, which further reduces the amount of energy we have available to properly function, encourages fat gain, and leads to the chronic diseases we see in epidemic proportions today.

We need to put an end to this terribly misguided approach to fat loss and health and instead shift our focus to the process of energy production. By increasing the amount of energy we produce, we can reduce the storage of food as body fat which will allow us to lose fat while also improving our health.

As I’m sure you’ve already gathered, there are quite a few factors affecting energy production. If you want to learn more about those factors and learn to lose fat the healthy way, sign up for the free mini-course below!

References

The Mythical Calorie Equation

Calories In – Calorie Out = Change in Body Fat

This ubiquitous equation represents the idea that the difference between the number of calories we consume and the number of calories we expend determines the amount of fat we gain or lose. It’s a wonderfully simple conception, although not an accurate one, and actually a very dangerous one.

It’s truly amazing to me that this equation has stuck around this long. The entire concept is illogical to begin with, not to mention the mounds of evidence against it.

Yet, the dogmatic adherence to this equation has informed so much of the current nutrition recommendations. This is especially true when it comes to fat loss, where “eat less and exercise more” is the common mantra. But it has also been applied to the general health recommendations to eat foods that are less calorie-dense, drink more water, and consume more protein and fiber to keep us full for longer, among many others.

While the fact that we associate calories with fat gain and loss is bad, the fact that we associate them with health is even worse.

But before we dive in too far, let’s start by exploring the extensive evidence that refutes the validity of equation.

Isocaloric Studies

If the calorie equation was valid, then consuming diets containing different foods with the same number of calories would have the same effects on body fat. But, many studies that have tested this hypothesis have shown that this isn’t the case. Let’s take a look at a few of them.

This first study, performed in a metabolic ward, had subjects on isocaloric reduced-fat or reduced-carbohydrate diets (1) (isocaloric means the diets had the same number of calories). They found that subjects on the reduced-fat diets lost more body fat than subjects on the reduced-carb diets. And, those on the reduced-fat diets lost less weight than those on the reduced-carb diets, meaning that a much higher percentage of the weight they lost was fat.

[This study also provides more evidence against the “burn fat for fat loss” fallacy, as those on the reduced-carb diets burned more fat than the reduced-fat group even though they lost less body fat.]

This next study also compared subjects on isocaloric diets with varying amounts of carbs and fat, although this one was performed on rats instead of humans (2). They found that the rats on the high-fat diets had higher total body fat by the end of the study than those on the control diet, but those on the high-carb diets didn’t. Again, remember that the high-fat and high-carb rats were fed the exact same number of calories!

In this study, human subjects were given 1 of 3 isocaloric diets that contained varying amounts of carbohydrates, and they found huge differences in weight loss, fat loss, and percent weight loss based on the amount of carbohydrates in the diet (3). In fact, those on the diet that was highest in carbohydrates lost 14 pounds more of body fat than those on the lowest carbohydrate diet during the 9-week intervention! In reference to these results, the authors commented that “no adequate explanation [could] be given for [the] weight loss differences.”

There are many more isocaloric studies that provide similar evidence against the calorie equation, including one on rats where two groups were fed the exact same diet except for the type of protein and ended up with a 26% difference in fat mass (4) and other studies showing that changing the amount of fat or carbohydrate in the diet affected the amount of body fat gained or lost, even when consuming the same number of calories (5, 6).

It’s clear based on these studies that the calorie equation isn’t quite as simple as it was made out to be. The types of foods that are eaten have a substantial effect on changes in body fat, rather than simply the number of “calories-in.”

Now, the argument can be made that changing the types of foods simply changes the number of “calories-out.” And, while this is true, it’s often entirely ignored in favor of the recommendations to simply “eat less and exercise more.”

Even when not ignored, the fact that the type of food, rather than simply the number of calories, affects the number of “calories-out” creates problems of its own.

It’s known that different diet compositions can vary in their metabolizable energy (the amount of energy in the food that’s actually digested and absorbed) and thermic effects (the amount of energy required for digesting and using the food). It’s also acknowledged that different diet compositions can cause changes in the resting metabolic rate and physical activity levels. But, some of the effects of different diet compositions can’t be fully explained yet.

This review, aimed at figuring out whether we can account for all the energetic effects of different diet compositions, looked at many calorie-controlled weight loss studies (7). They found that “neither macronutrient-specific differences in the availability of dietary energy nor changes in energy expenditure could explain [the] differences in weight loss” and concluded by suggesting that “further research is needed to identify the mechanisms that result in greater weight loss with one diet than with another.”

In other words, even if we account for differences in metabolizable energy, thermic effects, resting metabolic rate, and physical activity levels, (which very few people are doing) there are still unknown variables that would need to be factored in to make the calorie equation work.

This presents a glaring problem with this equation, but it doesn’t end here. There are other, more serious problems with the calorie equation that arise because it’s predicated on several false assumptions.

Caloric Restriction, Metabolic Adaptation, and Behavioral Compensation

The first of these assumptions is that our bodies’ energy usage doesn’t change based on our environment.

There have been many times where researchers have tried to apply the calorie equation to fat loss. They set up experiments where they reduce people’s food intakes and increase their exercise, thereby reducing the number of “calories-in” and increasing the number of “calories-out.”

And these studies do result in weight loss. But the amount of weight loss is nowhere near the amount predicted by the calorie equation.

This discrepancy boils down to two main factors:

1. Metabolic Adaptation

Metabolic adaptation is how our bodies internally adjust, or adapt, to changes in caloric intake (“calories-in”) or caloric expenditure (“calories-out”). When we reduce our caloric intake or increase our caloric expenditure, our bodies reduce the amount of energy they use. And when we increase our caloric intake or decrease our caloric expenditure, our bodies increase the amount of energy they use (8, 9, 10, 11).

This is accomplished through various hormonal and enzymatic changes, which allow for adjustments in energy usage, metabolic fuel selection, and energy partitioning.

These adaptive responses throw another wrench in the calorie equation. If we factor metabolic adaptation into the equation, we would have to reduce our caloric intake even more to achieve our desired weight loss.

2. Behavioral Compensation

Behavioral compensation is how we respond externally to changes in caloric intake or expenditure. This could mean reducing the amount we exercise when we eat fewer calories or increasing the amount we eat when we exercise more.

One review that considered many weight loss studies found that, because of behavioral compensation, the amount of weight loss from caloric restriction averages to be 12-44% less than what’s predicted by the calorie equation (12). They also found the amount of weight loss from increased exercise to be 55-64% less than was expected due to behavioral compensation.

Those are HUGE differences between the mythical calorie equation and reality!

And, behavioral compensation is an even bigger factor when we increase the amount of “calories-in.” The amount of weight gain in these situations is up to 96% less than is expected from the calorie equation! (12) You read that right, 96%! That basically means that we’re really good at compensating when we eat more food than normal, to the point that it’s pretty hard to gain weight that way.

But of course, metabolic adaptation and behavioral compensation don’t mean that the mythical equation is wrong. They’re just two more variables we have to factor into the equation that at this point is unrecognizable compared to the original “calories in – calories out = change in body fat.”

Up until this point we’ve only been dealing with adjustments to the calorie equation, but after considering this next false assumption it’ll become quite clear that this equation has no place in the health or fat loss arena.

What Are Calories?

This brings us to one of the most egregious errors that underlies the calorie equation: Calories are not relevant to human physiology.

Calories are simply a measure of energy, specifically heat energy.

In the context of nutrition, we think about the number of calories, or potential energy, held in certain foods. But, we can consider the number of calories in anything, whether it’s grass, wood, or gasoline.

Now, we all know that our bodies can’t convert the energy (calories) in grass, wood, or gasoline to usable energy in our bodies. So why do we assume that we’ll equally convert the energy in all food to usable energy in our bodies?

We consider that a mango has 200 calories, a steak has 600 calories, and a doughnut has 300 calories, but we don’t consider how much of that potential energy can or will be converted to usable energy.

There are many factors that affect how much of the energy, or calories, in the food we eat will become usable energy in our bodies.

The food must first be digested and absorbed. However, the amount of the food that actually gets digested and absorbed varies greatly based on the food and our gut function, and varying amounts of energy are required for this digestion and absorption.

Once absorbed, the carbohydrates, fats, and protein from the food we eat can be used to produce energy. This occurs in the mitochondria of our cells through a process called respiration.

During this process, the food we eat is converted into a form of usable energy that’s held in a molecule called ATP. But, there are tons of factors that affect whether the carbohydrates, fats, and protein even get to the mitochondria, let alone whether they’ll be used to produce ATP.

The different macronutrients (carbs, fats, and protein) vary significantly in this regard. Carbohydrates are our primary energy source while fat is our secondary energy source. Protein, on the other hand, is not likely to be converted to usable energy through mitochondrial respiration and is instead used primarily for building and rebuilding tissues.

So, it makes little sense to equate the potential energy, or calories, between the different macronutrients, as the likelihood that they’ll be used to produce ATP varies considerably. Equating the calories between the different macronutrients actually violates the second law of thermodynamics, as is explained here:

“A review of simple thermodynamic principles shows that weight change on isocaloric diets is not expected to be independent of path (metabolism of macronutrients) and indeed such a general principle would be a violation of the second law [of thermodynamics].” “The second law of thermodynamics says that variation of efficiency for different metabolic pathways is to be expected. Thus, ironically the dictum that a “calorie is a calorie” violates the second law of thermodynamics, as a matter of principle.” (13)

And, the factors that affect mitochondrial respiration go far beyond the differences between macronutrients. They also include the hormonal state, the amount of nutrients available, the toxins present, the time of day, the ambient temperature, the amount of sunlight present, the psychological state, and virtually every other aspect of our environment.

In other words, our bodies don’t run on a calorie currency, as they must convert the energy in food that we call “calories” into energy that they can use. And the amount of calories in our food is barely relevant considering the many factors that affect its conversion to usable energy.

The problems with the misplaced focus on calories has been nicely summed up in this quote:

“It is increasingly clear that the idea that “a calorie is a calorie” is misleading… Different diets… lead to different biochemical pathways (due to the hormonal and enzymatic changes) that are not equivalent when correctly compared through the laws of thermodynamics. Unless one measures heat and the biomolecules synthesized using ATP, it is inappropriate to assume that the only thing that counts in terms of food consumption and energy balance is the intake of dietary calories and weight storage.” (6)

And, as if all of this weren’t enough, the amount of usable energy that we do produce or use doesn’t say anything about where or what that energy is used for, which is vitally important to consider for both fat loss and health!

The Dangers of Caloric Restriction

The final false assumption of the calorie equation is that any excess energy we have will become fat, while any energy deficit will result in fat loss.

This assumption that fat gain is the product of excess energy and fat loss is the product of a lack of energy is probably the single most harmful misconception that exists in the health and nutrition field.

The 1st law of thermodynamics is often cited in support of this idea, which explains that energy cannot be created or destroyed. But, this has nothing to do with where energy is used or the physiological processes of fat gain and loss.

Energy is used for virtually everything we do. It’s used to accomplish our basic daily functions, like breathing and digesting, in addition to handling stressors, like exercise and mental work. Energy is also used to maintain, repair, and grow our tissues, like muscles, bones, fascia, and organs.

All the factors we’ve mentioned so far, including our hormonal state and the many aspects of our environment, determine the partitioning of energy, or where energy is used.

For example, in the rat study that was mentioned earlier, the amount of energy from consumed protein that was allocated to fat and muscle tissue differed based on the type of protein that was consumed (4).

However, the calorie equation doesn’t acknowledge the concept of energy partitioning and instead relies on the extremely common fallacy that any excess energy we have will be used for body fat and any energy deficit will come from body fat.

While this ignores a key physiological concept, there’s another problem with this fallacy that we haven’t addressed: body fat is a storage of fuel, or potential energy. In other words, the potential energy in food is stored as body fat when it’s NOT converted to usable energy.

While this is somewhat acknowledged, it’s assumed that energy production occurs until we have enough energy, at which point any potential energy left over becomes fat. But, that couldn’t be farther from the truth.

As was mentioned earlier, energy production, or mitochondrial respiration, is affected by all sorts of variables, from the amount of nutrients available to the time of day. When energy production is inhibited based on these many factors, the potential energy from our food is stored as fat and we’re left without enough energy to properly function.

This is what underlies fat gain and the obesity epidemic. Not too much energy, but too little energy (14).

As such, the recommendations to further reduce our available energy only make the problem worse, as is explained in this quote:

“In conclusion, the presented metabolic mechanism of environmentally caused obesity indicates energy deficiency as an engine working toward development of obesity. It is obvious that all efforts to stop this engine by further decreasing the energy cannot be successful. Thus, the low calorie diets and exercise regimens seem to be a redundant burden of already exhausted people.” (14)

Unfortunately, it doesn’t end there. Our bodies adapt to energy deficiencies by further inhibiting energy production and storing more fuel as fat in order to conserve energy, resulting in a vicious cycle (10, 14, 15).

This is the biggest reason why the calorie equation is destroying our health. We already lack energy due to the inhibition of mitochondrial respiration by nutrient deficiencies and many other problems, and then we eat less and exercise more, which further reduces the amount of energy we have available to properly function, encourages fat gain, and leads to the chronic diseases we see in epidemic proportions today.

We need to put an end to this terribly misguided approach to fat loss and health and instead shift our focus to the process of energy production. By increasing the amount of energy we produce, we can reduce the storage of food as body fat which will allow us to lose fat while also improving our health.

As I’m sure you’ve already gathered, there are quite a few factors affecting energy production. If you want to learn more about those factors and learn to lose fat the healthy way, sign up for the free mini-course below!

References

Omega-3s Are NOT The “Healthy Fats”

Omega-3s are all the rage nowadays.

Everybody’s taking fish oil – it’s the new miracle cure, featured on the news, on every health site, and in the supermarkets.

Foods like salmon, flaxseeds, and walnuts are considered the ultimate health foods because of their “heart-healthy” omega-3 fats, which are supposed to benefit everything from heart disease to diabetes to cancer.

And this is coupled with ridiculous claims of boosting the immune system, improving memory, and anti-aging effects.

But, omega-3s don’t have all the benefits that they’re claimed to have. They’ve been found not to protect against heart disease and stroke (1, 2, 3, 4, 5), cancer (4, 5), macular degeneration (6), IBD (7), aging (8), or dementia, Alzheimer’s disease, and other neurological disorders (9, 10).

Not only do omega-3s not benefit many of the diseases they’re claimed to, they also contribute to many of them.

But, before we get too carried away on all the problems omega-3s cause, let’s first talk about what omega-3s are, and how they differ from their omega-6 siblings.

 

Omega-3s vs. Omega-6s

Omega-3s and omega-6s are polyunsaturated fats. As I talked about in this article, these fats are incredibly harmful.

The omega-6 fats are mostly found in vegetable oils, nuts, and seeds, and were promoted as the healthy replacement for the “artery-clogging” saturated fats. But, it’s become more well-recognized that the omega-6 fats, which were once touted for their “heart-healthy” qualities and other supposed benefits, are harmful to our health.

The omega-3 fats, on the other hand, are found in fish, flaxseeds, chia seeds, walnuts, and some other foods. These fats have come onto the health scene more recently than the omega-6 fats and are now replacing them as the “healthy fats.”

As I explained in the aforementioned article, the polyunsaturated fats, including both the omega-3s and omega-6s, are harmful for 3 reasons:

  • They’re structurally weak
  • They’re converted into harmful, inflammatory compounds
  • They’re highly susceptible to damage

Well as it turns out, the omega-3s are even worse than the omega-6s when it comes to these 3 parameters.

 

You Thought Omega-6s Were Weak?

If you thought omega-6s were weak, just wait until you hear this.

The omega-3s have more double bonds than their omega-6 counterparts, making them even less stable. This leaves them structurally weaker and about twice as susceptible to damage than the omega-6s.

For example, DHA is one of the omega-3 fats that’s considered to be extremely beneficial. But, the amount of DHA used structurally in our cells is directly related to aging and lifespan (11). In other words, the more DHA in our cells, the faster we age and shorter we live.

This is because DHA is one of the weakest and least stable fats. When used as a structural component of the mitochondria, it increases the leakage of energy more than any other polyunsaturated fat (12). And, it’s 320 times more susceptible to damage than monounsaturated fats! (11)

As I mentioned in the last article on fats, when the polyunsaturated fats become damaged through lipid peroxidation they wreak havoc on the body. And, not only are omega-3s more susceptible to this damage, they’re also converted to compounds that are even more destructive.

When the omega-3s undergo lipid peroxidation they’re converted into hydroperoxides and endoperoxides. These compounds, as well as their reactive aldehyde breakdown products such as acrolein, HNE, and MDA, are extremely harmful.

These compounds damage proteins and DNA, including the cellular components that are needed for energy production (4, 13, 14, 15, 16). These compounds are also implicated in cancer, diabetes, heart disease, liver disease, Alzheimer’s disease, aging, and are known to be neurotoxic (16, 17, 18, 19, 20).

Now, the argument may be made that eating these polyunsaturated fats doesn’t mean that they’ll become damaged and cause this destruction. But, many studies have discredited this argument by showing that increased omega-3 consumption (and PUFA consumption in general) does increase lipid peroxidation and the presence of their harmful breakdown products (21, 22, 23, 24, 25, 26, 27, 28, 29).

 

Omega-3s Are NOT The “Healthy Fats”

Maybe it’s overkill by now, but just to hammer the point home…

Because of the damaging effects of omega-3s and their derivatives, omega-3s have been implicated in causing cancer (30, 31, 32, 33), fatty liver (34, 35, 36), and insulin resistance (37, 38). And, like the omega-6s, they’re also strongly immunosuppressive (39, 40, 41).

And, while the omega-3s are currently recommended during pregnancy and infancy, they’ve been shown to cause shorter lifespans, lower body weights, and neurological abnormalities in children whose mothers consumed large amounts of them (42).

So with all that being said, can we stop promoting the omega-3s as healthy already? Or are we going to have to wait another 30 years to figure it out?

And while we’re at it, maybe we should reconsider all the fish oil supplementation.

 

References

Omega-3s Are NOT The “Healthy Fats”

Omega-3s are all the rage nowadays.

Everybody’s taking fish oil – it’s the new miracle cure, featured on the news, on every health site, and in the supermarkets.

Foods like salmon, flaxseeds, and walnuts are considered the ultimate health foods because of their “heart-healthy” omega-3 fats, which are supposed to benefit everything from heart disease to diabetes to cancer.

And this is coupled with ridiculous claims of boosting the immune system, improving memory, and anti-aging effects.

But, omega-3s don’t have all the benefits that they’re claimed to have. They’ve been found not to protect against heart disease and stroke (1, 2, 3, 4, 5), cancer (4, 5), macular degeneration (6), IBD (7), aging (8), or dementia, Alzheimer’s disease, and other neurological disorders (9, 10).

Not only do omega-3s not benefit many of the diseases they’re claimed to, they also contribute to many of them.

But, before we get too carried away on all the problems omega-3s cause, let’s first talk about what omega-3s are, and how they differ from their omega-6 siblings.

 

Omega-3s vs. Omega-6s

Omega-3s and omega-6s are polyunsaturated fats. As I talked about in this article, these fats are incredibly harmful.

The omega-6 fats are mostly found in vegetable oils, nuts, and seeds, and were promoted as the healthy replacement for the “artery-clogging” saturated fats. But, it’s become more well-recognized that the omega-6 fats, which were once touted for their “heart-healthy” qualities and other supposed benefits, are harmful to our health.

The omega-3 fats, on the other hand, are found in fish, flaxseeds, chia seeds, walnuts, and some other foods. These fats have come onto the health scene more recently than the omega-6 fats and are now replacing them as the “healthy fats.”

As I explained in the aforementioned article, the polyunsaturated fats, including both the omega-3s and omega-6s, are harmful for 3 reasons:

  • They’re structurally weak
  • They’re converted into harmful, inflammatory compounds
  • They’re highly susceptible to damage

Well as it turns out, the omega-3s are even worse than the omega-6s when it comes to these 3 parameters.

 

You Thought Omega-6s Were Weak?

If you thought omega-6s were weak, just wait until you hear this.

The omega-3s have more double bonds than their omega-6 counterparts, making them even less stable. This leaves them structurally weaker and about twice as susceptible to damage than the omega-6s.

For example, DHA is one of the omega-3 fats that’s considered to be extremely beneficial. But, the amount of DHA used structurally in our cells is directly related to aging and lifespan (11). In other words, the more DHA in our cells, the faster we age and shorter we live.

This is because DHA is one of the weakest and least stable fats. When used as a structural component of the mitochondria, it increases the leakage of energy more than any other polyunsaturated fat (12). And, it’s 320 times more susceptible to damage than monounsaturated fats! (11)

As I mentioned in the last article on fats, when the polyunsaturated fats become damaged through lipid peroxidation they wreak havoc on the body. And, not only are omega-3s more susceptible to this damage, they’re also converted to compounds that are even more destructive.

When the omega-3s undergo lipid peroxidation they’re converted into hydroperoxides and endoperoxides. These compounds, as well as their reactive aldehyde breakdown products such as acrolein, HNE, and MDA, are extremely harmful.

These compounds damage proteins and DNA, including the cellular components that are needed for energy production (4, 13, 14, 15, 16). These compounds are also implicated in cancer, diabetes, heart disease, liver disease, Alzheimer’s disease, aging, and are known to be neurotoxic (16, 17, 18, 19, 20).

Now, the argument may be made that eating these polyunsaturated fats doesn’t mean that they’ll become damaged and cause this destruction. But, many studies have discredited this argument by showing that increased omega-3 consumption (and PUFA consumption in general) does increase lipid peroxidation and the presence of their harmful breakdown products (21, 22, 23, 24, 25, 26, 27, 28, 29).

 

Omega-3s Are NOT The “Healthy Fats”

Maybe it’s overkill by now, but just to hammer the point home…

Because of the damaging effects of omega-3s and their derivatives, omega-3s have been implicated in causing cancer (30, 31, 32, 33), fatty liver (34, 35, 36), and insulin resistance (37, 38). And, like the omega-6s, they’re also strongly immunosuppressive (39, 40, 41).

And, while the omega-3s are currently recommended during pregnancy and infancy, they’ve been shown to cause shorter lifespans, lower body weights, and neurological abnormalities in children whose mothers consumed large amounts of them (42).

So with all that being said, can we stop promoting the omega-3s as healthy already? Or are we going to have to wait another 30 years to figure it out?

And while we’re at it, maybe we should reconsider all the fish oil supplementation.

 

References

Omega-3s Are NOT The “Healthy Fats”

Omega-3s are all the rage nowadays.

Everybody’s taking fish oil – it’s the new miracle cure, featured on the news, on every health site, and in the supermarkets.

Foods like salmon, flaxseeds, and walnuts are considered the ultimate health foods because of their “heart-healthy” omega-3 fats, which are supposed to benefit everything from heart disease to diabetes to cancer.

And this is coupled with ridiculous claims of boosting the immune system, improving memory, and anti-aging effects.

But, omega-3s don’t have all the benefits that they’re claimed to have. They’ve been found not to protect against heart disease and stroke (1, 2, 3, 4, 5), cancer (4, 5), macular degeneration (6), IBD (7), aging (8), or dementia, Alzheimer’s disease, and other neurological disorders (9, 10).

Not only do omega-3s not benefit many of the diseases they’re claimed to, they also contribute to many of them.

But, before we get too carried away on all the problems omega-3s cause, let’s first talk about what omega-3s are, and how they differ from their omega-6 siblings.

 

Omega-3s vs. Omega-6s

Omega-3s and omega-6s are polyunsaturated fats. As I talked about in this article, these fats are incredibly harmful.

The omega-6 fats are mostly found in vegetable oils, nuts, and seeds, and were promoted as the healthy replacement for the “artery-clogging” saturated fats. But, it’s become more well-recognized that the omega-6 fats, which were once touted for their “heart-healthy” qualities and other supposed benefits, are harmful to our health.

The omega-3 fats, on the other hand, are found in fish, flaxseeds, chia seeds, walnuts, and some other foods. These fats have come onto the health scene more recently than the omega-6 fats and are now replacing them as the “healthy fats.”

As I explained in the aforementioned article, the polyunsaturated fats, including both the omega-3s and omega-6s, are harmful for 3 reasons:

  • They’re structurally weak
  • They’re converted into harmful, inflammatory compounds
  • They’re highly susceptible to damage

Well as it turns out, the omega-3s are even worse than the omega-6s when it comes to these 3 parameters.

 

You Thought Omega-6s Were Weak?

If you thought omega-6s were weak, just wait until you hear this.

The omega-3s have more double bonds than their omega-6 counterparts, making them even less stable. This leaves them structurally weaker and about twice as susceptible to damage than the omega-6s.

For example, DHA is one of the omega-3 fats that’s considered to be extremely beneficial. But, the amount of DHA used structurally in our cells is directly related to aging and lifespan (11). In other words, the more DHA in our cells, the faster we age and shorter we live.

This is because DHA is one of the weakest and least stable fats. When used as a structural component of the mitochondria, it increases the leakage of energy more than any other polyunsaturated fat (12). And, it’s 320 times more susceptible to damage than monounsaturated fats! (11)

As I mentioned in the last article on fats, when the polyunsaturated fats become damaged through lipid peroxidation they wreak havoc on the body. And, not only are omega-3s more susceptible to this damage, they’re also converted to compounds that are even more destructive.

When the omega-3s undergo lipid peroxidation they’re converted into hydroperoxides and endoperoxides. These compounds, as well as their reactive aldehyde breakdown products such as acrolein, HNE, and MDA, are extremely harmful.

These compounds damage proteins and DNA, including the cellular components that are needed for energy production (4, 13, 14, 15, 16). These compounds are also implicated in cancer, diabetes, heart disease, liver disease, Alzheimer’s disease, aging, and are known to be neurotoxic (16, 17, 18, 19, 20).

Now, the argument may be made that eating these polyunsaturated fats doesn’t mean that they’ll become damaged and cause this destruction. But, many studies have discredited this argument by showing that increased omega-3 consumption (and PUFA consumption in general) does increase lipid peroxidation and the presence of their harmful breakdown products (21, 22, 23, 24, 25, 26, 27, 28, 29).

 

Omega-3s Are NOT The “Healthy Fats”

Maybe it’s overkill by now, but just to hammer the point home…

Because of the damaging effects of omega-3s and their derivatives, omega-3s have been implicated in causing cancer (30, 31, 32, 33), fatty liver (34, 35, 36), and insulin resistance (37, 38). And, like the omega-6s, they’re also strongly immunosuppressive (39, 40, 41).

And, while the omega-3s are currently recommended during pregnancy and infancy, they’ve been shown to cause shorter lifespans, lower body weights, and neurological abnormalities in children whose mothers consumed large amounts of them (42).

So with all that being said, can we stop promoting the omega-3s as healthy already? Or are we going to have to wait another 30 years to figure it out?

And while we’re at it, maybe we should reconsider all the fish oil supplementation.

 

References

Omega-3s Are NOT The “Healthy Fats”

Omega-3s are all the rage nowadays.

Everybody’s taking fish oil – it’s the new miracle cure, featured on the news, on every health site, and in the supermarkets.

Foods like salmon, flaxseeds, and walnuts are considered the ultimate health foods because of their “heart-healthy” omega-3 fats, which are supposed to benefit everything from heart disease to diabetes to cancer.

And this is coupled with ridiculous claims of boosting the immune system, improving memory, and anti-aging effects.

But, omega-3s don’t have all the benefits that they’re claimed to have. They’ve been found not to protect against heart disease and stroke (1, 2, 3, 4, 5), cancer (4, 5), macular degeneration (6), IBD (7), aging (8), or dementia, Alzheimer’s disease, and other neurological disorders (9, 10).

Not only do omega-3s not benefit many of the diseases they’re claimed to, they also contribute to many of them.

But, before we get too carried away on all the problems omega-3s cause, let’s first talk about what omega-3s are, and how they differ from their omega-6 siblings.

 

Omega-3s vs. Omega-6s

Omega-3s and omega-6s are polyunsaturated fats. As I talked about in this article, these fats are incredibly harmful.

The omega-6 fats are mostly found in vegetable oils, nuts, and seeds, and were promoted as the healthy replacement for the “artery-clogging” saturated fats. But, it’s become more well-recognized that the omega-6 fats, which were once touted for their “heart-healthy” qualities and other supposed benefits, are harmful to our health.

The omega-3 fats, on the other hand, are found in fish, flaxseeds, chia seeds, walnuts, and some other foods. These fats have come onto the health scene more recently than the omega-6 fats and are now replacing them as the “healthy fats.”

As I explained in the aforementioned article, the polyunsaturated fats, including both the omega-3s and omega-6s, are harmful for 3 reasons:

  • They’re structurally weak
  • They’re converted into harmful, inflammatory compounds
  • They’re highly susceptible to damage

Well as it turns out, the omega-3s are even worse than the omega-6s when it comes to these 3 parameters.

 

You Thought Omega-6s Were Weak?

If you thought omega-6s were weak, just wait until you hear this.

The omega-3s have more double bonds than their omega-6 counterparts, making them even less stable. This leaves them structurally weaker and about twice as susceptible to damage than the omega-6s.

For example, DHA is one of the omega-3 fats that’s considered to be extremely beneficial. But, the amount of DHA used structurally in our cells is directly related to aging and lifespan (11). In other words, the more DHA in our cells, the faster we age and shorter we live.

This is because DHA is one of the weakest and least stable fats. When used as a structural component of the mitochondria, it increases the leakage of energy more than any other polyunsaturated fat (12). And, it’s 320 times more susceptible to damage than monounsaturated fats! (11)

As I mentioned in the last article on fats, when the polyunsaturated fats become damaged through lipid peroxidation they wreak havoc on the body. And, not only are omega-3s more susceptible to this damage, they’re also converted to compounds that are even more destructive.

When the omega-3s undergo lipid peroxidation they’re converted into hydroperoxides and endoperoxides. These compounds, as well as their reactive aldehyde breakdown products such as acrolein, HNE, and MDA, are extremely harmful.

These compounds damage proteins and DNA, including the cellular components that are needed for energy production (4, 13, 14, 15, 16). These compounds are also implicated in cancer, diabetes, heart disease, liver disease, Alzheimer’s disease, aging, and are known to be neurotoxic (16, 17, 18, 19, 20).

Now, the argument may be made that eating these polyunsaturated fats doesn’t mean that they’ll become damaged and cause this destruction. But, many studies have discredited this argument by showing that increased omega-3 consumption (and PUFA consumption in general) does increase lipid peroxidation and the presence of their harmful breakdown products (21, 22, 23, 24, 25, 26, 27, 28, 29).

 

Omega-3s Are NOT The “Healthy Fats”

Maybe it’s overkill by now, but just to hammer the point home…

Because of the damaging effects of omega-3s and their derivatives, omega-3s have been implicated in causing cancer (30, 31, 32, 33), fatty liver (34, 35, 36), and insulin resistance (37, 38). And, like the omega-6s, they’re also strongly immunosuppressive (39, 40, 41).

And, while the omega-3s are currently recommended during pregnancy and infancy, they’ve been shown to cause shorter lifespans, lower body weights, and neurological abnormalities in children whose mothers consumed large amounts of them (42).

So with all that being said, can we stop promoting the omega-3s as healthy already? Or are we going to have to wait another 30 years to figure it out?

And while we’re at it, maybe we should reconsider all the fish oil supplementation.

 

References

Omega-3s Are NOT The “Healthy Fats”

Omega-3s are all the rage nowadays.

Everybody’s taking fish oil – it’s the new miracle cure, featured on the news, on every health site, and in the supermarkets.

Foods like salmon, flaxseeds, and walnuts are considered the ultimate health foods because of their “heart-healthy” omega-3 fats, which are supposed to benefit everything from heart disease to diabetes to cancer.

And this is coupled with ridiculous claims of boosting the immune system, improving memory, and anti-aging effects.

But, omega-3s don’t have all the benefits that they’re claimed to have. They’ve been found not to protect against heart disease and stroke (1, 2, 3, 4, 5), cancer (4, 5), macular degeneration (6), IBD (7), aging (8), or dementia, Alzheimer’s disease, and other neurological disorders (9, 10).

Not only do omega-3s not benefit many of the diseases they’re claimed to, they also contribute to many of them.

But, before we get too carried away on all the problems omega-3s cause, let’s first talk about what omega-3s are, and how they differ from their omega-6 siblings.

 

Omega-3s vs. Omega-6s

Omega-3s and omega-6s are polyunsaturated fats. As I talked about in this article, these fats are incredibly harmful.

The omega-6 fats are mostly found in vegetable oils, nuts, and seeds, and were promoted as the healthy replacement for the “artery-clogging” saturated fats. But, it’s become more well-recognized that the omega-6 fats, which were once touted for their “heart-healthy” qualities and other supposed benefits, are harmful to our health.

The omega-3 fats, on the other hand, are found in fish, flaxseeds, chia seeds, walnuts, and some other foods. These fats have come onto the health scene more recently than the omega-6 fats and are now replacing them as the “healthy fats.”

As I explained in the aforementioned article, the polyunsaturated fats, including both the omega-3s and omega-6s, are harmful for 3 reasons:

  • They’re structurally weak
  • They’re converted into harmful, inflammatory compounds
  • They’re highly susceptible to damage

Well as it turns out, the omega-3s are even worse than the omega-6s when it comes to these 3 parameters.

 

You Thought Omega-6s Were Weak?

If you thought omega-6s were weak, just wait until you hear this.

The omega-3s have more double bonds than their omega-6 counterparts, making them even less stable. This leaves them structurally weaker and about twice as susceptible to damage than the omega-6s.

For example, DHA is one of the omega-3 fats that’s considered to be extremely beneficial. But, the amount of DHA used structurally in our cells is directly related to aging and lifespan (11). In other words, the more DHA in our cells, the faster we age and shorter we live.

This is because DHA is one of the weakest and least stable fats. When used as a structural component of the mitochondria, it increases the leakage of energy more than any other polyunsaturated fat (12). And, it’s 320 times more susceptible to damage than monounsaturated fats! (11)

As I mentioned in the last article on fats, when the polyunsaturated fats become damaged through lipid peroxidation they wreak havoc on the body. And, not only are omega-3s more susceptible to this damage, they’re also converted to compounds that are even more destructive.

When the omega-3s undergo lipid peroxidation they’re converted into hydroperoxides and endoperoxides. These compounds, as well as their reactive aldehyde breakdown products such as acrolein, HNE, and MDA, are extremely harmful.

These compounds damage proteins and DNA, including the cellular components that are needed for energy production (4, 13, 14, 15, 16). These compounds are also implicated in cancer, diabetes, heart disease, liver disease, Alzheimer’s disease, aging, and are known to be neurotoxic (16, 17, 18, 19, 20).

Now, the argument may be made that eating these polyunsaturated fats doesn’t mean that they’ll become damaged and cause this destruction. But, many studies have discredited this argument by showing that increased omega-3 consumption (and PUFA consumption in general) does increase lipid peroxidation and the presence of their harmful breakdown products (21, 22, 23, 24, 25, 26, 27, 28, 29).

 

Omega-3s Are NOT The “Healthy Fats”

Maybe it’s overkill by now, but just to hammer the point home…

Because of the damaging effects of omega-3s and their derivatives, omega-3s have been implicated in causing cancer (30, 31, 32, 33), fatty liver (34, 35, 36), and insulin resistance (37, 38). And, like the omega-6s, they’re also strongly immunosuppressive (39, 40, 41).

And, while the omega-3s are currently recommended during pregnancy and infancy, they’ve been shown to cause shorter lifespans, lower body weights, and neurological abnormalities in children whose mothers consumed large amounts of them (42).

So with all that being said, can we stop promoting the omega-3s as healthy already? Or are we going to have to wait another 30 years to figure it out?

And while we’re at it, maybe we should reconsider all the fish oil supplementation.

 

References

Omega-3s Are NOT The “Healthy Fats”

Omega-3s are all the rage nowadays.

Everybody’s taking fish oil – it’s the new miracle cure, featured on the news, on every health site, and in the supermarkets.

Foods like salmon, flaxseeds, and walnuts are considered the ultimate health foods because of their “heart-healthy” omega-3 fats, which are supposed to benefit everything from heart disease to diabetes to cancer.

And this is coupled with ridiculous claims of boosting the immune system, improving memory, and anti-aging effects.

But, omega-3s don’t have all the benefits that they’re claimed to have. They’ve been found not to protect against heart disease and stroke (1, 2, 3, 4, 5), cancer (4, 5), macular degeneration (6), IBD (7), aging (8), or dementia, Alzheimer’s disease, and other neurological disorders (9, 10).

Not only do omega-3s not benefit many of the diseases they’re claimed to, they also contribute to many of them.

But, before we get too carried away on all the problems omega-3s cause, let’s first talk about what omega-3s are, and how they differ from their omega-6 siblings.

 

Omega-3s vs. Omega-6s

Omega-3s and omega-6s are polyunsaturated fats. As I talked about in this article, these fats are incredibly harmful.

The omega-6 fats are mostly found in vegetable oils, nuts, and seeds, and were promoted as the healthy replacement for the “artery-clogging” saturated fats. But, it’s become more well-recognized that the omega-6 fats, which were once touted for their “heart-healthy” qualities and other supposed benefits, are harmful to our health.

The omega-3 fats, on the other hand, are found in fish, flaxseeds, chia seeds, walnuts, and some other foods. These fats have come onto the health scene more recently than the omega-6 fats and are now replacing them as the “healthy fats.”

As I explained in the aforementioned article, the polyunsaturated fats, including both the omega-3s and omega-6s, are harmful for 3 reasons:

  • They’re structurally weak
  • They’re converted into harmful, inflammatory compounds
  • They’re highly susceptible to damage

Well as it turns out, the omega-3s are even worse than the omega-6s when it comes to these 3 parameters.

 

You Thought Omega-6s Were Weak?

If you thought omega-6s were weak, just wait until you hear this.

The omega-3s have more double bonds than their omega-6 counterparts, making them even less stable. This leaves them structurally weaker and about twice as susceptible to damage than the omega-6s.

For example, DHA is one of the omega-3 fats that’s considered to be extremely beneficial. But, the amount of DHA used structurally in our cells is directly related to aging and lifespan (11). In other words, the more DHA in our cells, the faster we age and shorter we live.

This is because DHA is one of the weakest and least stable fats. When used as a structural component of the mitochondria, it increases the leakage of energy more than any other polyunsaturated fat (12). And, it’s 320 times more susceptible to damage than monounsaturated fats! (11)

As I mentioned in the last article on fats, when the polyunsaturated fats become damaged through lipid peroxidation they wreak havoc on the body. And, not only are omega-3s more susceptible to this damage, they’re also converted to compounds that are even more destructive.

When the omega-3s undergo lipid peroxidation they’re converted into hydroperoxides and endoperoxides. These compounds, as well as their reactive aldehyde breakdown products such as acrolein, HNE, and MDA, are extremely harmful.

These compounds damage proteins and DNA, including the cellular components that are needed for energy production (4, 13, 14, 15, 16). These compounds are also implicated in cancer, diabetes, heart disease, liver disease, Alzheimer’s disease, aging, and are known to be neurotoxic (16, 17, 18, 19, 20).

Now, the argument may be made that eating these polyunsaturated fats doesn’t mean that they’ll become damaged and cause this destruction. But, many studies have discredited this argument by showing that increased omega-3 consumption (and PUFA consumption in general) does increase lipid peroxidation and the presence of their harmful breakdown products (21, 22, 23, 24, 25, 26, 27, 28, 29).

 

Omega-3s Are NOT The “Healthy Fats”

Maybe it’s overkill by now, but just to hammer the point home…

Because of the damaging effects of omega-3s and their derivatives, omega-3s have been implicated in causing cancer (30, 31, 32, 33), fatty liver (34, 35, 36), and insulin resistance (37, 38). And, like the omega-6s, they’re also strongly immunosuppressive (39, 40, 41).

And, while the omega-3s are currently recommended during pregnancy and infancy, they’ve been shown to cause shorter lifespans, lower body weights, and neurological abnormalities in children whose mothers consumed large amounts of them (42).

So with all that being said, can we stop promoting the omega-3s as healthy already? Or are we going to have to wait another 30 years to figure it out?

And while we’re at it, maybe we should reconsider all the fish oil supplementation.

 

References

Omega-3s Are NOT The “Healthy Fats”

Omega-3s are all the rage nowadays.

Everybody’s taking fish oil – it’s the new miracle cure, featured on the news, on every health site, and in the supermarkets.

Foods like salmon, flaxseeds, and walnuts are considered the ultimate health foods because of their “heart-healthy” omega-3 fats, which are supposed to benefit everything from heart disease to diabetes to cancer.

And this is coupled with ridiculous claims of boosting the immune system, improving memory, and anti-aging effects.

But, omega-3s don’t have all the benefits that they’re claimed to have. They’ve been found not to protect against heart disease and stroke (1, 2, 3, 4, 5), cancer (4, 5), macular degeneration (6), IBD (7), aging (8), or dementia, Alzheimer’s disease, and other neurological disorders (9, 10).

Not only do omega-3s not benefit many of the diseases they’re claimed to, they also contribute to many of them.

But, before we get too carried away on all the problems omega-3s cause, let’s first talk about what omega-3s are, and how they differ from their omega-6 siblings.

 

Omega-3s vs. Omega-6s

Omega-3s and omega-6s are polyunsaturated fats. As I talked about in this article, these fats are incredibly harmful.

The omega-6 fats are mostly found in vegetable oils, nuts, and seeds, and were promoted as the healthy replacement for the “artery-clogging” saturated fats. But, it’s become more well-recognized that the omega-6 fats, which were once touted for their “heart-healthy” qualities and other supposed benefits, are harmful to our health.

The omega-3 fats, on the other hand, are found in fish, flaxseeds, chia seeds, walnuts, and some other foods. These fats have come onto the health scene more recently than the omega-6 fats and are now replacing them as the “healthy fats.”

As I explained in the aforementioned article, the polyunsaturated fats, including both the omega-3s and omega-6s, are harmful for 3 reasons:

  • They’re structurally weak
  • They’re converted into harmful, inflammatory compounds
  • They’re highly susceptible to damage

Well as it turns out, the omega-3s are even worse than the omega-6s when it comes to these 3 parameters.

 

You Thought Omega-6s Were Weak?

If you thought omega-6s were weak, just wait until you hear this.

The omega-3s have more double bonds than their omega-6 counterparts, making them even less stable. This leaves them structurally weaker and about twice as susceptible to damage than the omega-6s.

For example, DHA is one of the omega-3 fats that’s considered to be extremely beneficial. But, the amount of DHA used structurally in our cells is directly related to aging and lifespan (11). In other words, the more DHA in our cells, the faster we age and shorter we live.

This is because DHA is one of the weakest and least stable fats. When used as a structural component of the mitochondria, it increases the leakage of energy more than any other polyunsaturated fat (12). And, it’s 320 times more susceptible to damage than monounsaturated fats! (11)

As I mentioned in the last article on fats, when the polyunsaturated fats become damaged through lipid peroxidation they wreak havoc on the body. And, not only are omega-3s more susceptible to this damage, they’re also converted to compounds that are even more destructive.

When the omega-3s undergo lipid peroxidation they’re converted into hydroperoxides and endoperoxides. These compounds, as well as their reactive aldehyde breakdown products such as acrolein, HNE, and MDA, are extremely harmful.

These compounds damage proteins and DNA, including the cellular components that are needed for energy production (4, 13, 14, 15, 16). These compounds are also implicated in cancer, diabetes, heart disease, liver disease, Alzheimer’s disease, aging, and are known to be neurotoxic (16, 17, 18, 19, 20).

Now, the argument may be made that eating these polyunsaturated fats doesn’t mean that they’ll become damaged and cause this destruction. But, many studies have discredited this argument by showing that increased omega-3 consumption (and PUFA consumption in general) does increase lipid peroxidation and the presence of their harmful breakdown products (21, 22, 23, 24, 25, 26, 27, 28, 29).

 

Omega-3s Are NOT The “Healthy Fats”

Maybe it’s overkill by now, but just to hammer the point home…

Because of the damaging effects of omega-3s and their derivatives, omega-3s have been implicated in causing cancer (30, 31, 32, 33), fatty liver (34, 35, 36), and insulin resistance (37, 38). And, like the omega-6s, they’re also strongly immunosuppressive (39, 40, 41).

And, while the omega-3s are currently recommended during pregnancy and infancy, they’ve been shown to cause shorter lifespans, lower body weights, and neurological abnormalities in children whose mothers consumed large amounts of them (42).

So with all that being said, can we stop promoting the omega-3s as healthy already? Or are we going to have to wait another 30 years to figure it out?

And while we’re at it, maybe we should reconsider all the fish oil supplementation.

 

References

Omega-3s Are NOT The “Healthy Fats”

Omega-3s are all the rage nowadays.

Everybody’s taking fish oil – it’s the new miracle cure, featured on the news, on every health site, and in the supermarkets.

Foods like salmon, flaxseeds, and walnuts are considered the ultimate health foods because of their “heart-healthy” omega-3 fats, which are supposed to benefit everything from heart disease to diabetes to cancer.

And this is coupled with ridiculous claims of boosting the immune system, improving memory, and anti-aging effects.

But, omega-3s don’t have all the benefits that they’re claimed to have. They’ve been found not to protect against heart disease and stroke (1, 2, 3, 4, 5), cancer (4, 5), macular degeneration (6), IBD (7), aging (8), or dementia, Alzheimer’s disease, and other neurological disorders (9, 10).

Not only do omega-3s not benefit many of the diseases they’re claimed to, they also contribute to many of them.

But, before we get too carried away on all the problems omega-3s cause, let’s first talk about what omega-3s are, and how they differ from their omega-6 siblings.

 

Omega-3s vs. Omega-6s

Omega-3s and omega-6s are polyunsaturated fats. As I talked about in this article, these fats are incredibly harmful.

The omega-6 fats are mostly found in vegetable oils, nuts, and seeds, and were promoted as the healthy replacement for the “artery-clogging” saturated fats. But, it’s become more well-recognized that the omega-6 fats, which were once touted for their “heart-healthy” qualities and other supposed benefits, are harmful to our health.

The omega-3 fats, on the other hand, are found in fish, flaxseeds, chia seeds, walnuts, and some other foods. These fats have come onto the health scene more recently than the omega-6 fats and are now replacing them as the “healthy fats.”

As I explained in the aforementioned article, the polyunsaturated fats, including both the omega-3s and omega-6s, are harmful for 3 reasons:

  • They’re structurally weak
  • They’re converted into harmful, inflammatory compounds
  • They’re highly susceptible to damage

Well as it turns out, the omega-3s are even worse than the omega-6s when it comes to these 3 parameters.

 

You Thought Omega-6s Were Weak?

If you thought omega-6s were weak, just wait until you hear this.

The omega-3s have more double bonds than their omega-6 counterparts, making them even less stable. This leaves them structurally weaker and about twice as susceptible to damage than the omega-6s.

For example, DHA is one of the omega-3 fats that’s considered to be extremely beneficial. But, the amount of DHA used structurally in our cells is directly related to aging and lifespan (11). In other words, the more DHA in our cells, the faster we age and shorter we live.

This is because DHA is one of the weakest and least stable fats. When used as a structural component of the mitochondria, it increases the leakage of energy more than any other polyunsaturated fat (12). And, it’s 320 times more susceptible to damage than monounsaturated fats! (11)

As I mentioned in the last article on fats, when the polyunsaturated fats become damaged through lipid peroxidation they wreak havoc on the body. And, not only are omega-3s more susceptible to this damage, they’re also converted to compounds that are even more destructive.

When the omega-3s undergo lipid peroxidation they’re converted into hydroperoxides and endoperoxides. These compounds, as well as their reactive aldehyde breakdown products such as acrolein, HNE, and MDA, are extremely harmful.

These compounds damage proteins and DNA, including the cellular components that are needed for energy production (4, 13, 14, 15, 16). These compounds are also implicated in cancer, diabetes, heart disease, liver disease, Alzheimer’s disease, aging, and are known to be neurotoxic (16, 17, 18, 19, 20).

Now, the argument may be made that eating these polyunsaturated fats doesn’t mean that they’ll become damaged and cause this destruction. But, many studies have discredited this argument by showing that increased omega-3 consumption (and PUFA consumption in general) does increase lipid peroxidation and the presence of their harmful breakdown products (21, 22, 23, 24, 25, 26, 27, 28, 29).

 

Omega-3s Are NOT The “Healthy Fats”

Maybe it’s overkill by now, but just to hammer the point home…

Because of the damaging effects of omega-3s and their derivatives, omega-3s have been implicated in causing cancer (30, 31, 32, 33), fatty liver (34, 35, 36), and insulin resistance (37, 38). And, like the omega-6s, they’re also strongly immunosuppressive (39, 40, 41).

And, while the omega-3s are currently recommended during pregnancy and infancy, they’ve been shown to cause shorter lifespans, lower body weights, and neurological abnormalities in children whose mothers consumed large amounts of them (42).

So with all that being said, can we stop promoting the omega-3s as healthy already? Or are we going to have to wait another 30 years to figure it out?

And while we’re at it, maybe we should reconsider all the fish oil supplementation.

 

References

Omega-3s Are NOT The “Healthy Fats”

Omega-3s are all the rage nowadays.

Everybody’s taking fish oil – it’s the new miracle cure, featured on the news, on every health site, and in the supermarkets.

Foods like salmon, flaxseeds, and walnuts are considered the ultimate health foods because of their “heart-healthy” omega-3 fats, which are supposed to benefit everything from heart disease to diabetes to cancer.

And this is coupled with ridiculous claims of boosting the immune system, improving memory, and anti-aging effects.

But, omega-3s don’t have all the benefits that they’re claimed to have. They’ve been found not to protect against heart disease and stroke (1, 2, 3, 4, 5), cancer (4, 5), macular degeneration (6), IBD (7), aging (8), or dementia, Alzheimer’s disease, and other neurological disorders (9, 10).

Not only do omega-3s not benefit many of the diseases they’re claimed to, they also contribute to many of them.

But, before we get too carried away on all the problems omega-3s cause, let’s first talk about what omega-3s are, and how they differ from their omega-6 siblings.

 

Omega-3s vs. Omega-6s

Omega-3s and omega-6s are polyunsaturated fats. As I talked about in this article, these fats are incredibly harmful.

The omega-6 fats are mostly found in vegetable oils, nuts, and seeds, and were promoted as the healthy replacement for the “artery-clogging” saturated fats. But, it’s become more well-recognized that the omega-6 fats, which were once touted for their “heart-healthy” qualities and other supposed benefits, are harmful to our health.

The omega-3 fats, on the other hand, are found in fish, flaxseeds, chia seeds, walnuts, and some other foods. These fats have come onto the health scene more recently than the omega-6 fats and are now replacing them as the “healthy fats.”

As I explained in the aforementioned article, the polyunsaturated fats, including both the omega-3s and omega-6s, are harmful for 3 reasons:

  • They’re structurally weak
  • They’re converted into harmful, inflammatory compounds
  • They’re highly susceptible to damage

Well as it turns out, the omega-3s are even worse than the omega-6s when it comes to these 3 parameters.

 

You Thought Omega-6s Were Weak?

If you thought omega-6s were weak, just wait until you hear this.

The omega-3s have more double bonds than their omega-6 counterparts, making them even less stable. This leaves them structurally weaker and about twice as susceptible to damage than the omega-6s.

For example, DHA is one of the omega-3 fats that’s considered to be extremely beneficial. But, the amount of DHA used structurally in our cells is directly related to aging and lifespan (11). In other words, the more DHA in our cells, the faster we age and shorter we live.

This is because DHA is one of the weakest and least stable fats. When used as a structural component of the mitochondria, it increases the leakage of energy more than any other polyunsaturated fat (12). And, it’s 320 times more susceptible to damage than monounsaturated fats! (11)

As I mentioned in the last article on fats, when the polyunsaturated fats become damaged through lipid peroxidation they wreak havoc on the body. And, not only are omega-3s more susceptible to this damage, they’re also converted to compounds that are even more destructive.

When the omega-3s undergo lipid peroxidation they’re converted into hydroperoxides and endoperoxides. These compounds, as well as their reactive aldehyde breakdown products such as acrolein, HNE, and MDA, are extremely harmful.

These compounds damage proteins and DNA, including the cellular components that are needed for energy production (4, 13, 14, 15, 16). These compounds are also implicated in cancer, diabetes, heart disease, liver disease, Alzheimer’s disease, aging, and are known to be neurotoxic (16, 17, 18, 19, 20).

Now, the argument may be made that eating these polyunsaturated fats doesn’t mean that they’ll become damaged and cause this destruction. But, many studies have discredited this argument by showing that increased omega-3 consumption (and PUFA consumption in general) does increase lipid peroxidation and the presence of their harmful breakdown products (21, 22, 23, 24, 25, 26, 27, 28, 29).

 

Omega-3s Are NOT The “Healthy Fats”

Maybe it’s overkill by now, but just to hammer the point home…

Because of the damaging effects of omega-3s and their derivatives, omega-3s have been implicated in causing cancer (30, 31, 32, 33), fatty liver (34, 35, 36), and insulin resistance (37, 38). And, like the omega-6s, they’re also strongly immunosuppressive (39, 40, 41).

And, while the omega-3s are currently recommended during pregnancy and infancy, they’ve been shown to cause shorter lifespans, lower body weights, and neurological abnormalities in children whose mothers consumed large amounts of them (42).

So with all that being said, can we stop promoting the omega-3s as healthy already? Or are we going to have to wait another 30 years to figure it out?

And while we’re at it, maybe we should reconsider all the fish oil supplementation.

 

References

Omega-3s Are NOT The “Healthy Fats”

Omega-3s are all the rage nowadays.

Everybody’s taking fish oil – it’s the new miracle cure, featured on the news, on every health site, and in the supermarkets.

Foods like salmon, flaxseeds, and walnuts are considered the ultimate health foods because of their “heart-healthy” omega-3 fats, which are supposed to benefit everything from heart disease to diabetes to cancer.

And this is coupled with ridiculous claims of boosting the immune system, improving memory, and anti-aging effects.

But, omega-3s don’t have all the benefits that they’re claimed to have. They’ve been found not to protect against heart disease and stroke (1, 2, 3, 4, 5), cancer (4, 5), macular degeneration (6), IBD (7), aging (8), or dementia, Alzheimer’s disease, and other neurological disorders (9, 10).

Not only do omega-3s not benefit many of the diseases they’re claimed to, they also contribute to many of them.

But, before we get too carried away on all the problems omega-3s cause, let’s first talk about what omega-3s are, and how they differ from their omega-6 siblings.

 

Omega-3s vs. Omega-6s

Omega-3s and omega-6s are polyunsaturated fats. As I talked about in this article, these fats are incredibly harmful.

The omega-6 fats are mostly found in vegetable oils, nuts, and seeds, and were promoted as the healthy replacement for the “artery-clogging” saturated fats. But, it’s become more well-recognized that the omega-6 fats, which were once touted for their “heart-healthy” qualities and other supposed benefits, are harmful to our health.

The omega-3 fats, on the other hand, are found in fish, flaxseeds, chia seeds, walnuts, and some other foods. These fats have come onto the health scene more recently than the omega-6 fats and are now replacing them as the “healthy fats.”

As I explained in the aforementioned article, the polyunsaturated fats, including both the omega-3s and omega-6s, are harmful for 3 reasons:

  • They’re structurally weak
  • They’re converted into harmful, inflammatory compounds
  • They’re highly susceptible to damage

Well as it turns out, the omega-3s are even worse than the omega-6s when it comes to these 3 parameters.

 

You Thought Omega-6s Were Weak?

If you thought omega-6s were weak, just wait until you hear this.

The omega-3s have more double bonds than their omega-6 counterparts, making them even less stable. This leaves them structurally weaker and about twice as susceptible to damage than the omega-6s.

For example, DHA is one of the omega-3 fats that’s considered to be extremely beneficial. But, the amount of DHA used structurally in our cells is directly related to aging and lifespan (11). In other words, the more DHA in our cells, the faster we age and shorter we live.

This is because DHA is one of the weakest and least stable fats. When used as a structural component of the mitochondria, it increases the leakage of energy more than any other polyunsaturated fat (12). And, it’s 320 times more susceptible to damage than monounsaturated fats! (11)

As I mentioned in the last article on fats, when the polyunsaturated fats become damaged through lipid peroxidation they wreak havoc on the body. And, not only are omega-3s more susceptible to this damage, they’re also converted to compounds that are even more destructive.

When the omega-3s undergo lipid peroxidation they’re converted into hydroperoxides and endoperoxides. These compounds, as well as their reactive aldehyde breakdown products such as acrolein, HNE, and MDA, are extremely harmful.

These compounds damage proteins and DNA, including the cellular components that are needed for energy production (4, 13, 14, 15, 16). These compounds are also implicated in cancer, diabetes, heart disease, liver disease, Alzheimer’s disease, aging, and are known to be neurotoxic (16, 17, 18, 19, 20).

Now, the argument may be made that eating these polyunsaturated fats doesn’t mean that they’ll become damaged and cause this destruction. But, many studies have discredited this argument by showing that increased omega-3 consumption (and PUFA consumption in general) does increase lipid peroxidation and the presence of their harmful breakdown products (21, 22, 23, 24, 25, 26, 27, 28, 29).

 

Omega-3s Are NOT The “Healthy Fats”

Maybe it’s overkill by now, but just to hammer the point home…

Because of the damaging effects of omega-3s and their derivatives, omega-3s have been implicated in causing cancer (30, 31, 32, 33), fatty liver (34, 35, 36), and insulin resistance (37, 38). And, like the omega-6s, they’re also strongly immunosuppressive (39, 40, 41).

And, while the omega-3s are currently recommended during pregnancy and infancy, they’ve been shown to cause shorter lifespans, lower body weights, and neurological abnormalities in children whose mothers consumed large amounts of them (42).

So with all that being said, can we stop promoting the omega-3s as healthy already? Or are we going to have to wait another 30 years to figure it out?

And while we’re at it, maybe we should reconsider all the fish oil supplementation.

 

References

Omega-3s Are NOT The “Healthy Fats”

Omega-3s are all the rage nowadays.

Everybody’s taking fish oil – it’s the new miracle cure, featured on the news, on every health site, and in the supermarkets.

Foods like salmon, flaxseeds, and walnuts are considered the ultimate health foods because of their “heart-healthy” omega-3 fats, which are supposed to benefit everything from heart disease to diabetes to cancer.

And this is coupled with ridiculous claims of boosting the immune system, improving memory, and anti-aging effects.

But, omega-3s don’t have all the benefits that they’re claimed to have. They’ve been found not to protect against heart disease and stroke (1, 2, 3, 4, 5), cancer (4, 5), macular degeneration (6), IBD (7), aging (8), or dementia, Alzheimer’s disease, and other neurological disorders (9, 10).

Not only do omega-3s not benefit many of the diseases they’re claimed to, they also contribute to many of them.

But, before we get too carried away on all the problems omega-3s cause, let’s first talk about what omega-3s are, and how they differ from their omega-6 siblings.

 

Omega-3s vs. Omega-6s

Omega-3s and omega-6s are polyunsaturated fats. As I talked about in this article, these fats are incredibly harmful.

The omega-6 fats are mostly found in vegetable oils, nuts, and seeds, and were promoted as the healthy replacement for the “artery-clogging” saturated fats. But, it’s become more well-recognized that the omega-6 fats, which were once touted for their “heart-healthy” qualities and other supposed benefits, are harmful to our health.

The omega-3 fats, on the other hand, are found in fish, flaxseeds, chia seeds, walnuts, and some other foods. These fats have come onto the health scene more recently than the omega-6 fats and are now replacing them as the “healthy fats.”

As I explained in the aforementioned article, the polyunsaturated fats, including both the omega-3s and omega-6s, are harmful for 3 reasons:

  • They’re structurally weak
  • They’re converted into harmful, inflammatory compounds
  • They’re highly susceptible to damage

Well as it turns out, the omega-3s are even worse than the omega-6s when it comes to these 3 parameters.

 

You Thought Omega-6s Were Weak?

If you thought omega-6s were weak, just wait until you hear this.

The omega-3s have more double bonds than their omega-6 counterparts, making them even less stable. This leaves them structurally weaker and about twice as susceptible to damage than the omega-6s.

For example, DHA is one of the omega-3 fats that’s considered to be extremely beneficial. But, the amount of DHA used structurally in our cells is directly related to aging and lifespan (11). In other words, the more DHA in our cells, the faster we age and shorter we live.

This is because DHA is one of the weakest and least stable fats. When used as a structural component of the mitochondria, it increases the leakage of energy more than any other polyunsaturated fat (12). And, it’s 320 times more susceptible to damage than monounsaturated fats! (11)

As I mentioned in the last article on fats, when the polyunsaturated fats become damaged through lipid peroxidation they wreak havoc on the body. And, not only are omega-3s more susceptible to this damage, they’re also converted to compounds that are even more destructive.

When the omega-3s undergo lipid peroxidation they’re converted into hydroperoxides and endoperoxides. These compounds, as well as their reactive aldehyde breakdown products such as acrolein, HNE, and MDA, are extremely harmful.

These compounds damage proteins and DNA, including the cellular components that are needed for energy production (4, 13, 14, 15, 16). These compounds are also implicated in cancer, diabetes, heart disease, liver disease, Alzheimer’s disease, aging, and are known to be neurotoxic (16, 17, 18, 19, 20).

Now, the argument may be made that eating these polyunsaturated fats doesn’t mean that they’ll become damaged and cause this destruction. But, many studies have discredited this argument by showing that increased omega-3 consumption (and PUFA consumption in general) does increase lipid peroxidation and the presence of their harmful breakdown products (21, 22, 23, 24, 25, 26, 27, 28, 29).

 

Omega-3s Are NOT The “Healthy Fats”

Maybe it’s overkill by now, but just to hammer the point home…

Because of the damaging effects of omega-3s and their derivatives, omega-3s have been implicated in causing cancer (30, 31, 32, 33), fatty liver (34, 35, 36), and insulin resistance (37, 38). And, like the omega-6s, they’re also strongly immunosuppressive (39, 40, 41).

And, while the omega-3s are currently recommended during pregnancy and infancy, they’ve been shown to cause shorter lifespans, lower body weights, and neurological abnormalities in children whose mothers consumed large amounts of them (42).

So with all that being said, can we stop promoting the omega-3s as healthy already? Or are we going to have to wait another 30 years to figure it out?

And while we’re at it, maybe we should reconsider all the fish oil supplementation.

 

References

Omega-3s Are NOT The “Healthy Fats”

Omega-3s are all the rage nowadays.

Everybody’s taking fish oil – it’s the new miracle cure, featured on the news, on every health site, and in the supermarkets.

Foods like salmon, flaxseeds, and walnuts are considered the ultimate health foods because of their “heart-healthy” omega-3 fats, which are supposed to benefit everything from heart disease to diabetes to cancer.

And this is coupled with ridiculous claims of boosting the immune system, improving memory, and anti-aging effects.

But, omega-3s don’t have all the benefits that they’re claimed to have. They’ve been found not to protect against heart disease and stroke (1, 2, 3, 4, 5), cancer (4, 5), macular degeneration (6), IBD (7), aging (8), or dementia, Alzheimer’s disease, and other neurological disorders (9, 10).

Not only do omega-3s not benefit many of the diseases they’re claimed to, they also contribute to many of them.

But, before we get too carried away on all the problems omega-3s cause, let’s first talk about what omega-3s are, and how they differ from their omega-6 siblings.

 

Omega-3s vs. Omega-6s

Omega-3s and omega-6s are polyunsaturated fats. As I talked about in this article, these fats are incredibly harmful.

The omega-6 fats are mostly found in vegetable oils, nuts, and seeds, and were promoted as the healthy replacement for the “artery-clogging” saturated fats. But, it’s become more well-recognized that the omega-6 fats, which were once touted for their “heart-healthy” qualities and other supposed benefits, are harmful to our health.

The omega-3 fats, on the other hand, are found in fish, flaxseeds, chia seeds, walnuts, and some other foods. These fats have come onto the health scene more recently than the omega-6 fats and are now replacing them as the “healthy fats.”

As I explained in the aforementioned article, the polyunsaturated fats, including both the omega-3s and omega-6s, are harmful for 3 reasons:

  • They’re structurally weak
  • They’re converted into harmful, inflammatory compounds
  • They’re highly susceptible to damage

Well as it turns out, the omega-3s are even worse than the omega-6s when it comes to these 3 parameters.

 

You Thought Omega-6s Were Weak?

If you thought omega-6s were weak, just wait until you hear this.

The omega-3s have more double bonds than their omega-6 counterparts, making them even less stable. This leaves them structurally weaker and about twice as susceptible to damage than the omega-6s.

For example, DHA is one of the omega-3 fats that’s considered to be extremely beneficial. But, the amount of DHA used structurally in our cells is directly related to aging and lifespan (11). In other words, the more DHA in our cells, the faster we age and shorter we live.

This is because DHA is one of the weakest and least stable fats. When used as a structural component of the mitochondria, it increases the leakage of energy more than any other polyunsaturated fat (12). And, it’s 320 times more susceptible to damage than monounsaturated fats! (11)

As I mentioned in the last article on fats, when the polyunsaturated fats become damaged through lipid peroxidation they wreak havoc on the body. And, not only are omega-3s more susceptible to this damage, they’re also converted to compounds that are even more destructive.

When the omega-3s undergo lipid peroxidation they’re converted into hydroperoxides and endoperoxides. These compounds, as well as their reactive aldehyde breakdown products such as acrolein, HNE, and MDA, are extremely harmful.

These compounds damage proteins and DNA, including the cellular components that are needed for energy production (4, 13, 14, 15, 16). These compounds are also implicated in cancer, diabetes, heart disease, liver disease, Alzheimer’s disease, aging, and are known to be neurotoxic (16, 17, 18, 19, 20).

Now, the argument may be made that eating these polyunsaturated fats doesn’t mean that they’ll become damaged and cause this destruction. But, many studies have discredited this argument by showing that increased omega-3 consumption (and PUFA consumption in general) does increase lipid peroxidation and the presence of their harmful breakdown products (21, 22, 23, 24, 25, 26, 27, 28, 29).

 

Omega-3s Are NOT The “Healthy Fats”

Maybe it’s overkill by now, but just to hammer the point home…

Because of the damaging effects of omega-3s and their derivatives, omega-3s have been implicated in causing cancer (30, 31, 32, 33), fatty liver (34, 35, 36), and insulin resistance (37, 38). And, like the omega-6s, they’re also strongly immunosuppressive (39, 40, 41).

And, while the omega-3s are currently recommended during pregnancy and infancy, they’ve been shown to cause shorter lifespans, lower body weights, and neurological abnormalities in children whose mothers consumed large amounts of them (42).

So with all that being said, can we stop promoting the omega-3s as healthy already? Or are we going to have to wait another 30 years to figure it out?

And while we’re at it, maybe we should reconsider all the fish oil supplementation.

 

References

Omega-3s Are NOT The “Healthy Fats”

Omega-3s are all the rage nowadays.

Everybody’s taking fish oil – it’s the new miracle cure, featured on the news, on every health site, and in the supermarkets.

Foods like salmon, flaxseeds, and walnuts are considered the ultimate health foods because of their “heart-healthy” omega-3 fats, which are supposed to benefit everything from heart disease to diabetes to cancer.

And this is coupled with ridiculous claims of boosting the immune system, improving memory, and anti-aging effects.

But, omega-3s don’t have all the benefits that they’re claimed to have. They’ve been found not to protect against heart disease and stroke (1, 2, 3, 4, 5), cancer (4, 5), macular degeneration (6), IBD (7), aging (8), or dementia, Alzheimer’s disease, and other neurological disorders (9, 10).

Not only do omega-3s not benefit many of the diseases they’re claimed to, they also contribute to many of them.

But, before we get too carried away on all the problems omega-3s cause, let’s first talk about what omega-3s are, and how they differ from their omega-6 siblings.

 

Omega-3s vs. Omega-6s

Omega-3s and omega-6s are polyunsaturated fats. As I talked about in this article, these fats are incredibly harmful.

The omega-6 fats are mostly found in vegetable oils, nuts, and seeds, and were promoted as the healthy replacement for the “artery-clogging” saturated fats. But, it’s become more well-recognized that the omega-6 fats, which were once touted for their “heart-healthy” qualities and other supposed benefits, are harmful to our health.

The omega-3 fats, on the other hand, are found in fish, flaxseeds, chia seeds, walnuts, and some other foods. These fats have come onto the health scene more recently than the omega-6 fats and are now replacing them as the “healthy fats.”

As I explained in the aforementioned article, the polyunsaturated fats, including both the omega-3s and omega-6s, are harmful for 3 reasons:

  • They’re structurally weak
  • They’re converted into harmful, inflammatory compounds
  • They’re highly susceptible to damage

Well as it turns out, the omega-3s are even worse than the omega-6s when it comes to these 3 parameters.

 

You Thought Omega-6s Were Weak?

If you thought omega-6s were weak, just wait until you hear this.

The omega-3s have more double bonds than their omega-6 counterparts, making them even less stable. This leaves them structurally weaker and about twice as susceptible to damage than the omega-6s.

For example, DHA is one of the omega-3 fats that’s considered to be extremely beneficial. But, the amount of DHA used structurally in our cells is directly related to aging and lifespan (11). In other words, the more DHA in our cells, the faster we age and shorter we live.

This is because DHA is one of the weakest and least stable fats. When used as a structural component of the mitochondria, it increases the leakage of energy more than any other polyunsaturated fat (12). And, it’s 320 times more susceptible to damage than monounsaturated fats! (11)

As I mentioned in the last article on fats, when the polyunsaturated fats become damaged through lipid peroxidation they wreak havoc on the body. And, not only are omega-3s more susceptible to this damage, they’re also converted to compounds that are even more destructive.

When the omega-3s undergo lipid peroxidation they’re converted into hydroperoxides and endoperoxides. These compounds, as well as their reactive aldehyde breakdown products such as acrolein, HNE, and MDA, are extremely harmful.

These compounds damage proteins and DNA, including the cellular components that are needed for energy production (4, 13, 14, 15, 16). These compounds are also implicated in cancer, diabetes, heart disease, liver disease, Alzheimer’s disease, aging, and are known to be neurotoxic (16, 17, 18, 19, 20).

Now, the argument may be made that eating these polyunsaturated fats doesn’t mean that they’ll become damaged and cause this destruction. But, many studies have discredited this argument by showing that increased omega-3 consumption (and PUFA consumption in general) does increase lipid peroxidation and the presence of their harmful breakdown products (21, 22, 23, 24, 25, 26, 27, 28, 29).

 

Omega-3s Are NOT The “Healthy Fats”

Maybe it’s overkill by now, but just to hammer the point home…

Because of the damaging effects of omega-3s and their derivatives, omega-3s have been implicated in causing cancer (30, 31, 32, 33), fatty liver (34, 35, 36), and insulin resistance (37, 38). And, like the omega-6s, they’re also strongly immunosuppressive (39, 40, 41).

And, while the omega-3s are currently recommended during pregnancy and infancy, they’ve been shown to cause shorter lifespans, lower body weights, and neurological abnormalities in children whose mothers consumed large amounts of them (42).

So with all that being said, can we stop promoting the omega-3s as healthy already? Or are we going to have to wait another 30 years to figure it out?

And while we’re at it, maybe we should reconsider all the fish oil supplementation.

 

References

Fats: We’ve Got It All Wrong

Somehow, the USDA still tells us not to consume more than 10% of our calories from saturated fat (1).

This is after they removed their recommendations to limit dietary cholesterol, and 4 years after TIME magazine declared that the war on fat had ended with a photo of butter on the cover and the mantra “Eat Butter” underneath.

In the TIME article they detailed how fat, specifically saturated fat, “has been the most vilified nutrient in the American diet” and that “our demonization of fat may have backfired in ways we are just beginning to understand.”

Yet, the battle against the evil, artery-clogging saturated fat rages on.

The article also explains the extremely flawed science that began the anti-saturated fat nonsense and details the lack of connection between saturated fat and heart disease. (Saturated fat has been blamed for heart disease because it raises LDL levels, although I explain the problems with this idea here.)

But while I agree with these points, if the TIME magazine article is any indication, we’re still completely lost when it comes to fats. The article shifts the blame to sugar, which I’ve already written several articles defending, and also touts the benefits of the polyunsaturated fats.

Herein lies an even bigger problem.

Not only are we still recommended to reduce our saturated fat consumption, we’re encouraged to replace these saturated fats with unsaturated fat, specifically the polyunsaturated fats.

 

What Are Polyunsaturated Fats?

While saturated fats are known as the heart-disease-causing fats, polyunsaturated fats are typically considered the “heart-healthy” fats.

Polyunsaturated fats, or PUFA, are the omega-3 and omega-6 fats that we’ve been encouraged to consume in place of the saturated fats. They’re found in fatty fish like salmon, nuts & seeds, and the vegetable oils that come from those nuts and seeds.

But, while the saturated fats have more or less been vindicated of their “artery-clogging” accusations, the general stance towards PUFA hasn’t changed. They’re still considered the angels of the fat world.

But, unlike the saturated fats, the polyunsaturated fats do contribute to heart disease (2, 3, 4, 5).

And they also contribute to virtually all other chronic conditions, including obesity & diabetes (6, 7), cancer (2, 8), fatty liver (9), and Alzheimer’s & Parkinson’s disease (10, 11, 12). This is not to mention that they’re also strongly immunosuppressive (13, 14, 15, 16).

So, how is it that these fats are so incredibly harmful?

Polyunsaturated fats have multiple double bonds in their carbon chains. This is what separates them from saturated fats, which don’t have any double bonds in their carbon chains.

The presence of double bonds in PUFA might sound like a minor detail, but it ends up causing problems at the most fundamental level of our health: energy balance.

Polyunsaturated fats inhibit energy production, drastically increase energy demands, and reduce the efficiency of energy usage.

These effects are so powerful that, beyond contributing to the chronic conditions I just mentioned, the PUFA content in our cells is also the primary determinant of lifespan and aging in all animals, including us humans! (17)

The reasons for these effects comes down to 3 properties of PUFA:

  • They’re structurally weak
  • They’re converted into harmful, inflammatory compounds
  • They’re highly susceptible to damage

Let’s explore each of these properties a little more.

 

Polyunsaturated fats are structurally weak

We often only consider the fats we eat as sources of energy. But, fats serve functional and structural purposes as well.

As structural components of the cell, fats are extremely important for holding energy and allowing our cells to properly function.

This leads us to one of the major problems that results from consuming PUFA.

When we consume PUFA, they’re incorporated as structural components in our cells, including their mitochondria (18). But, the presence of double bonds in PUFA makes them weak, so they serve as extremely poor structural components.

As poor structural components, PUFA cause our cells, or more specifically our mitochondria, to leak energy! (19, 20, 21, 22, 23). And in addition to leaking energy, they also cause our cells to leak out ions like potassium (21).

When taken together, these two effects drastically increase our energy demands and reduce the efficiency of energy usage.

 

Polyunsaturated fats are converted into harmful, inflammatory compounds

When not used structurally, PUFA can be converted into various compounds, like the eicosanoids.

The eicosanoids are the major compounds responsible for inflammation in the body. These are the compounds that the various anti-inflammatory medications, like aspirin and ibuprofen, block.

Chronic inflammation is one of the primary markers of chronic disease, and this chronic inflammation requires PUFA. In other words, reducing PUFA consumption is a great way to reduce inflammation.

But, it doesn’t end there.

PUFA can be converted into many other compounds that directly inhibit energy production (24, 25, 26, 27) and contribute to stress (28, 29).

Again, these effects are disastrous for energy balance.

 

Polyunsaturated fats are highly susceptible to damage

The first 2 properties of PUFA have been predicated on the fats remaining intact. But, because of the double bonds in these fats, they’re extremely susceptible to damage through a process called lipid peroxidation (17).

And this damage wreaks havoc in our body.

The peroxidation of PUFA causes oxidative stress and inflammation throughout our cells, which directly inhibits energy production and even damages the DNA and protein structure of our cells (17, 30).

Because of this extensive damage, lipid peroxidation is considered to be a crucial step in the development of many chronic conditions (31).

 

Saturated fats to the rescue

Even individually, these 3 properties of PUFA make them incredibly harmful. And given all of them together, I would stay as far away from these fats as possible.

But this is easier said than done.

These fats are probably the biggest contributor to the health problems we’re seeing today, and they are EVERYWHERE!

They’re found in many baked goods, processed foods, cooking oils, fake butters & margarines, salad dressings, and fried foods. Plus, they’re encouraged as health foods in the form of nuts & seeds, fatty fish, and fatty chicken and pork.

But luckily, all the harmful properties of PUFA are directly contrasted by the saturated fats.

Saturated fats are everything PUFA are not. They’re stable, so they don’t leak energy and are extremely resistant to damage, and they aren’t converted to dangerous compounds. And, they even protect against the effects of PUFA! (32)

So, replacing PUFA with saturated (and monounsaturated) fats like butter and coconut oil will go a long way for improving energy balance.

While it might go without saying, reducing or avoiding PUFA might take a bit of work. But it’s well worth it if you care about your health.

 

References

Fats: We’ve Got It All Wrong

Somehow, the USDA still tells us not to consume more than 10% of our calories from saturated fat (1).

This is after they removed their recommendations to limit dietary cholesterol, and 4 years after TIME magazine declared that the war on fat had ended with a photo of butter on the cover and the mantra “Eat Butter” underneath.

In the TIME article they detailed how fat, specifically saturated fat, “has been the most vilified nutrient in the American diet” and that “our demonization of fat may have backfired in ways we are just beginning to understand.”

Yet, the battle against the evil, artery-clogging saturated fat rages on.

The article also explains the extremely flawed science that began the anti-saturated fat nonsense and details the lack of connection between saturated fat and heart disease. (Saturated fat has been blamed for heart disease because it raises LDL levels, although I explain the problems with this idea here.)

But while I agree with these points, if the TIME magazine article is any indication, we’re still completely lost when it comes to fats. The article shifts the blame to sugar, which I’ve already written several articles defending, and also touts the benefits of the polyunsaturated fats.

Herein lies an even bigger problem.

Not only are we still recommended to reduce our saturated fat consumption, we’re encouraged to replace these saturated fats with unsaturated fat, specifically the polyunsaturated fats.

 

What Are Polyunsaturated Fats?

While saturated fats are known as the heart-disease-causing fats, polyunsaturated fats are typically considered the “heart-healthy” fats.

Polyunsaturated fats, or PUFA, are the omega-3 and omega-6 fats that we’ve been encouraged to consume in place of the saturated fats. They’re found in fatty fish like salmon, nuts & seeds, and the vegetable oils that come from those nuts and seeds.

But, while the saturated fats have more or less been vindicated of their “artery-clogging” accusations, the general stance towards PUFA hasn’t changed. They’re still considered the angels of the fat world.

But, unlike the saturated fats, the polyunsaturated fats do contribute to heart disease (2, 3, 4, 5).

And they also contribute to virtually all other chronic conditions, including obesity & diabetes (6, 7), cancer (2, 8), fatty liver (9), and Alzheimer’s & Parkinson’s disease (10, 11, 12). This is not to mention that they’re also strongly immunosuppressive (13, 14, 15, 16).

So, how is it that these fats are so incredibly harmful?

Polyunsaturated fats have multiple double bonds in their carbon chains. This is what separates them from saturated fats, which don’t have any double bonds in their carbon chains.

The presence of double bonds in PUFA might sound like a minor detail, but it ends up causing problems at the most fundamental level of our health: energy balance.

Polyunsaturated fats inhibit energy production, drastically increase energy demands, and reduce the efficiency of energy usage.

These effects are so powerful that, beyond contributing to the chronic conditions I just mentioned, the PUFA content in our cells is also the primary determinant of lifespan and aging in all animals, including us humans! (17)

The reasons for these effects comes down to 3 properties of PUFA:

  • They’re structurally weak
  • They’re converted into harmful, inflammatory compounds
  • They’re highly susceptible to damage

Let’s explore each of these properties a little more.

 

Polyunsaturated fats are structurally weak

We often only consider the fats we eat as sources of energy. But, fats serve functional and structural purposes as well.

As structural components of the cell, fats are extremely important for holding energy and allowing our cells to properly function.

This leads us to one of the major problems that results from consuming PUFA.

When we consume PUFA, they’re incorporated as structural components in our cells, including their mitochondria (18). But, the presence of double bonds in PUFA makes them weak, so they serve as extremely poor structural components.

As poor structural components, PUFA cause our cells, or more specifically our mitochondria, to leak energy! (19, 20, 21, 22, 23). And in addition to leaking energy, they also cause our cells to leak out ions like potassium (21).

When taken together, these two effects drastically increase our energy demands and reduce the efficiency of energy usage.

 

Polyunsaturated fats are converted into harmful, inflammatory compounds

When not used structurally, PUFA can be converted into various compounds, like the eicosanoids.

The eicosanoids are the major compounds responsible for inflammation in the body. These are the compounds that the various anti-inflammatory medications, like aspirin and ibuprofen, block.

Chronic inflammation is one of the primary markers of chronic disease, and this chronic inflammation requires PUFA. In other words, reducing PUFA consumption is a great way to reduce inflammation.

But, it doesn’t end there.

PUFA can be converted into many other compounds that directly inhibit energy production (24, 25, 26, 27) and contribute to stress (28, 29).

Again, these effects are disastrous for energy balance.

 

Polyunsaturated fats are highly susceptible to damage

The first 2 properties of PUFA have been predicated on the fats remaining intact. But, because of the double bonds in these fats, they’re extremely susceptible to damage through a process called lipid peroxidation (17).

And this damage wreaks havoc in our body.

The peroxidation of PUFA causes oxidative stress and inflammation throughout our cells, which directly inhibits energy production and even damages the DNA and protein structure of our cells (17, 30).

Because of this extensive damage, lipid peroxidation is considered to be a crucial step in the development of many chronic conditions (31).

 

Saturated fats to the rescue

Even individually, these 3 properties of PUFA make them incredibly harmful. And given all of them together, I would stay as far away from these fats as possible.

But this is easier said than done.

These fats are probably the biggest contributor to the health problems we’re seeing today, and they are EVERYWHERE!

They’re found in many baked goods, processed foods, cooking oils, fake butters & margarines, salad dressings, and fried foods. Plus, they’re encouraged as health foods in the form of nuts & seeds, fatty fish, and fatty chicken and pork.

But luckily, all the harmful properties of PUFA are directly contrasted by the saturated fats.

Saturated fats are everything PUFA are not. They’re stable, so they don’t leak energy and are extremely resistant to damage, and they aren’t converted to dangerous compounds. And, they even protect against the effects of PUFA! (32)

So, replacing PUFA with saturated (and monounsaturated) fats like butter and coconut oil will go a long way for improving energy balance.

While it might go without saying, reducing or avoiding PUFA might take a bit of work. But it’s well worth it if you care about your health.

 

References

Fats: We’ve Got It All Wrong

Somehow, the USDA still tells us not to consume more than 10% of our calories from saturated fat (1).

This is after they removed their recommendations to limit dietary cholesterol, and 4 years after TIME magazine declared that the war on fat had ended with a photo of butter on the cover and the mantra “Eat Butter” underneath.

In the TIME article they detailed how fat, specifically saturated fat, “has been the most vilified nutrient in the American diet” and that “our demonization of fat may have backfired in ways we are just beginning to understand.”

Yet, the battle against the evil, artery-clogging saturated fat rages on.

The article also explains the extremely flawed science that began the anti-saturated fat nonsense and details the lack of connection between saturated fat and heart disease. (Saturated fat has been blamed for heart disease because it raises LDL levels, although I explain the problems with this idea here.)

But while I agree with these points, if the TIME magazine article is any indication, we’re still completely lost when it comes to fats. The article shifts the blame to sugar, which I’ve already written several articles defending, and also touts the benefits of the polyunsaturated fats.

Herein lies an even bigger problem.

Not only are we still recommended to reduce our saturated fat consumption, we’re encouraged to replace these saturated fats with unsaturated fat, specifically the polyunsaturated fats.

 

What Are Polyunsaturated Fats?

While saturated fats are known as the heart-disease-causing fats, polyunsaturated fats are typically considered the “heart-healthy” fats.

Polyunsaturated fats, or PUFA, are the omega-3 and omega-6 fats that we’ve been encouraged to consume in place of the saturated fats. They’re found in fatty fish like salmon, nuts & seeds, and the vegetable oils that come from those nuts and seeds.

But, while the saturated fats have more or less been vindicated of their “artery-clogging” accusations, the general stance towards PUFA hasn’t changed. They’re still considered the angels of the fat world.

But, unlike the saturated fats, the polyunsaturated fats do contribute to heart disease (2, 3, 4, 5).

And they also contribute to virtually all other chronic conditions, including obesity & diabetes (6, 7), cancer (2, 8), fatty liver (9), and Alzheimer’s & Parkinson’s disease (10, 11, 12). This is not to mention that they’re also strongly immunosuppressive (13, 14, 15, 16).

So, how is it that these fats are so incredibly harmful?

Polyunsaturated fats have multiple double bonds in their carbon chains. This is what separates them from saturated fats, which don’t have any double bonds in their carbon chains.

The presence of double bonds in PUFA might sound like a minor detail, but it ends up causing problems at the most fundamental level of our health: energy balance.

Polyunsaturated fats inhibit energy production, drastically increase energy demands, and reduce the efficiency of energy usage.

These effects are so powerful that, beyond contributing to the chronic conditions I just mentioned, the PUFA content in our cells is also the primary determinant of lifespan and aging in all animals, including us humans! (17)

The reasons for these effects comes down to 3 properties of PUFA:

  • They’re structurally weak
  • They’re converted into harmful, inflammatory compounds
  • They’re highly susceptible to damage

Let’s explore each of these properties a little more.

 

Polyunsaturated fats are structurally weak

We often only consider the fats we eat as sources of energy. But, fats serve functional and structural purposes as well.

As structural components of the cell, fats are extremely important for holding energy and allowing our cells to properly function.

This leads us to one of the major problems that results from consuming PUFA.

When we consume PUFA, they’re incorporated as structural components in our cells, including their mitochondria (18). But, the presence of double bonds in PUFA makes them weak, so they serve as extremely poor structural components.

As poor structural components, PUFA cause our cells, or more specifically our mitochondria, to leak energy! (19, 20, 21, 22, 23). And in addition to leaking energy, they also cause our cells to leak out ions like potassium (21).

When taken together, these two effects drastically increase our energy demands and reduce the efficiency of energy usage.

 

Polyunsaturated fats are converted into harmful, inflammatory compounds

When not used structurally, PUFA can be converted into various compounds, like the eicosanoids.

The eicosanoids are the major compounds responsible for inflammation in the body. These are the compounds that the various anti-inflammatory medications, like aspirin and ibuprofen, block.

Chronic inflammation is one of the primary markers of chronic disease, and this chronic inflammation requires PUFA. In other words, reducing PUFA consumption is a great way to reduce inflammation.

But, it doesn’t end there.

PUFA can be converted into many other compounds that directly inhibit energy production (24, 25, 26, 27) and contribute to stress (28, 29).

Again, these effects are disastrous for energy balance.

 

Polyunsaturated fats are highly susceptible to damage

The first 2 properties of PUFA have been predicated on the fats remaining intact. But, because of the double bonds in these fats, they’re extremely susceptible to damage through a process called lipid peroxidation (17).

And this damage wreaks havoc in our body.

The peroxidation of PUFA causes oxidative stress and inflammation throughout our cells, which directly inhibits energy production and even damages the DNA and protein structure of our cells (17, 30).

Because of this extensive damage, lipid peroxidation is considered to be a crucial step in the development of many chronic conditions (31).

 

Saturated fats to the rescue

Even individually, these 3 properties of PUFA make them incredibly harmful. And given all of them together, I would stay as far away from these fats as possible.

But this is easier said than done.

These fats are probably the biggest contributor to the health problems we’re seeing today, and they are EVERYWHERE!

They’re found in many baked goods, processed foods, cooking oils, fake butters & margarines, salad dressings, and fried foods. Plus, they’re encouraged as health foods in the form of nuts & seeds, fatty fish, and fatty chicken and pork.

But luckily, all the harmful properties of PUFA are directly contrasted by the saturated fats.

Saturated fats are everything PUFA are not. They’re stable, so they don’t leak energy and are extremely resistant to damage, and they aren’t converted to dangerous compounds. And, they even protect against the effects of PUFA! (32)

So, replacing PUFA with saturated (and monounsaturated) fats like butter and coconut oil will go a long way for improving energy balance.

While it might go without saying, reducing or avoiding PUFA might take a bit of work. But it’s well worth it if you care about your health.

 

References

Fats: We’ve Got It All Wrong

Somehow, the USDA still tells us not to consume more than 10% of our calories from saturated fat (1).

This is after they removed their recommendations to limit dietary cholesterol, and 4 years after TIME magazine declared that the war on fat had ended with a photo of butter on the cover and the mantra “Eat Butter” underneath.

In the TIME article they detailed how fat, specifically saturated fat, “has been the most vilified nutrient in the American diet” and that “our demonization of fat may have backfired in ways we are just beginning to understand.”

Yet, the battle against the evil, artery-clogging saturated fat rages on.

The article also explains the extremely flawed science that began the anti-saturated fat nonsense and details the lack of connection between saturated fat and heart disease. (Saturated fat has been blamed for heart disease because it raises LDL levels, although I explain the problems with this idea here.)

But while I agree with these points, if the TIME magazine article is any indication, we’re still completely lost when it comes to fats. The article shifts the blame to sugar, which I’ve already written several articles defending, and also touts the benefits of the polyunsaturated fats.

Herein lies an even bigger problem.

Not only are we still recommended to reduce our saturated fat consumption, we’re encouraged to replace these saturated fats with unsaturated fat, specifically the polyunsaturated fats.

 

What Are Polyunsaturated Fats?

While saturated fats are known as the heart-disease-causing fats, polyunsaturated fats are typically considered the “heart-healthy” fats.

Polyunsaturated fats, or PUFA, are the omega-3 and omega-6 fats that we’ve been encouraged to consume in place of the saturated fats. They’re found in fatty fish like salmon, nuts & seeds, and the vegetable oils that come from those nuts and seeds.

But, while the saturated fats have more or less been vindicated of their “artery-clogging” accusations, the general stance towards PUFA hasn’t changed. They’re still considered the angels of the fat world.

But, unlike the saturated fats, the polyunsaturated fats do contribute to heart disease (2, 3, 4, 5).

And they also contribute to virtually all other chronic conditions, including obesity & diabetes (6, 7), cancer (2, 8), fatty liver (9), and Alzheimer’s & Parkinson’s disease (10, 11, 12). This is not to mention that they’re also strongly immunosuppressive (13, 14, 15, 16).

So, how is it that these fats are so incredibly harmful?

Polyunsaturated fats have multiple double bonds in their carbon chains. This is what separates them from saturated fats, which don’t have any double bonds in their carbon chains.

The presence of double bonds in PUFA might sound like a minor detail, but it ends up causing problems at the most fundamental level of our health: energy balance.

Polyunsaturated fats inhibit energy production, drastically increase energy demands, and reduce the efficiency of energy usage.

These effects are so powerful that, beyond contributing to the chronic conditions I just mentioned, the PUFA content in our cells is also the primary determinant of lifespan and aging in all animals, including us humans! (17)

The reasons for these effects comes down to 3 properties of PUFA:

  • They’re structurally weak
  • They’re converted into harmful, inflammatory compounds
  • They’re highly susceptible to damage

Let’s explore each of these properties a little more.

 

Polyunsaturated fats are structurally weak

We often only consider the fats we eat as sources of energy. But, fats serve functional and structural purposes as well.

As structural components of the cell, fats are extremely important for holding energy and allowing our cells to properly function.

This leads us to one of the major problems that results from consuming PUFA.

When we consume PUFA, they’re incorporated as structural components in our cells, including their mitochondria (18). But, the presence of double bonds in PUFA makes them weak, so they serve as extremely poor structural components.

As poor structural components, PUFA cause our cells, or more specifically our mitochondria, to leak energy! (19, 20, 21, 22, 23). And in addition to leaking energy, they also cause our cells to leak out ions like potassium (21).

When taken together, these two effects drastically increase our energy demands and reduce the efficiency of energy usage.

 

Polyunsaturated fats are converted into harmful, inflammatory compounds

When not used structurally, PUFA can be converted into various compounds, like the eicosanoids.

The eicosanoids are the major compounds responsible for inflammation in the body. These are the compounds that the various anti-inflammatory medications, like aspirin and ibuprofen, block.

Chronic inflammation is one of the primary markers of chronic disease, and this chronic inflammation requires PUFA. In other words, reducing PUFA consumption is a great way to reduce inflammation.

But, it doesn’t end there.

PUFA can be converted into many other compounds that directly inhibit energy production (24, 25, 26, 27) and contribute to stress (28, 29).

Again, these effects are disastrous for energy balance.

 

Polyunsaturated fats are highly susceptible to damage

The first 2 properties of PUFA have been predicated on the fats remaining intact. But, because of the double bonds in these fats, they’re extremely susceptible to damage through a process called lipid peroxidation (17).

And this damage wreaks havoc in our body.

The peroxidation of PUFA causes oxidative stress and inflammation throughout our cells, which directly inhibits energy production and even damages the DNA and protein structure of our cells (17, 30).

Because of this extensive damage, lipid peroxidation is considered to be a crucial step in the development of many chronic conditions (31).

 

Saturated fats to the rescue

Even individually, these 3 properties of PUFA make them incredibly harmful. And given all of them together, I would stay as far away from these fats as possible.

But this is easier said than done.

These fats are probably the biggest contributor to the health problems we’re seeing today, and they are EVERYWHERE!

They’re found in many baked goods, processed foods, cooking oils, fake butters & margarines, salad dressings, and fried foods. Plus, they’re encouraged as health foods in the form of nuts & seeds, fatty fish, and fatty chicken and pork.

But luckily, all the harmful properties of PUFA are directly contrasted by the saturated fats.

Saturated fats are everything PUFA are not. They’re stable, so they don’t leak energy and are extremely resistant to damage, and they aren’t converted to dangerous compounds. And, they even protect against the effects of PUFA! (32)

So, replacing PUFA with saturated (and monounsaturated) fats like butter and coconut oil will go a long way for improving energy balance.

While it might go without saying, reducing or avoiding PUFA might take a bit of work. But it’s well worth it if you care about your health.

 

References

Fats: We’ve Got It All Wrong

Somehow, the USDA still tells us not to consume more than 10% of our calories from saturated fat (1).

This is after they removed their recommendations to limit dietary cholesterol, and 4 years after TIME magazine declared that the war on fat had ended with a photo of butter on the cover and the mantra “Eat Butter” underneath.

In the TIME article they detailed how fat, specifically saturated fat, “has been the most vilified nutrient in the American diet” and that “our demonization of fat may have backfired in ways we are just beginning to understand.”

Yet, the battle against the evil, artery-clogging saturated fat rages on.

The article also explains the extremely flawed science that began the anti-saturated fat nonsense and details the lack of connection between saturated fat and heart disease. (Saturated fat has been blamed for heart disease because it raises LDL levels, although I explain the problems with this idea here.)

But while I agree with these points, if the TIME magazine article is any indication, we’re still completely lost when it comes to fats. The article shifts the blame to sugar, which I’ve already written several articles defending, and also touts the benefits of the polyunsaturated fats.

Herein lies an even bigger problem.

Not only are we still recommended to reduce our saturated fat consumption, we’re encouraged to replace these saturated fats with unsaturated fat, specifically the polyunsaturated fats.

 

What Are Polyunsaturated Fats?

While saturated fats are known as the heart-disease-causing fats, polyunsaturated fats are typically considered the “heart-healthy” fats.

Polyunsaturated fats, or PUFA, are the omega-3 and omega-6 fats that we’ve been encouraged to consume in place of the saturated fats. They’re found in fatty fish like salmon, nuts & seeds, and the vegetable oils that come from those nuts and seeds.

But, while the saturated fats have more or less been vindicated of their “artery-clogging” accusations, the general stance towards PUFA hasn’t changed. They’re still considered the angels of the fat world.

But, unlike the saturated fats, the polyunsaturated fats do contribute to heart disease (2, 3, 4, 5).

And they also contribute to virtually all other chronic conditions, including obesity & diabetes (6, 7), cancer (2, 8), fatty liver (9), and Alzheimer’s & Parkinson’s disease (10, 11, 12). This is not to mention that they’re also strongly immunosuppressive (13, 14, 15, 16).

So, how is it that these fats are so incredibly harmful?

Polyunsaturated fats have multiple double bonds in their carbon chains. This is what separates them from saturated fats, which don’t have any double bonds in their carbon chains.

The presence of double bonds in PUFA might sound like a minor detail, but it ends up causing problems at the most fundamental level of our health: energy balance.

Polyunsaturated fats inhibit energy production, drastically increase energy demands, and reduce the efficiency of energy usage.

These effects are so powerful that, beyond contributing to the chronic conditions I just mentioned, the PUFA content in our cells is also the primary determinant of lifespan and aging in all animals, including us humans! (17)

The reasons for these effects comes down to 3 properties of PUFA:

  • They’re structurally weak
  • They’re converted into harmful, inflammatory compounds
  • They’re highly susceptible to damage

Let’s explore each of these properties a little more.

 

Polyunsaturated fats are structurally weak

We often only consider the fats we eat as sources of energy. But, fats serve functional and structural purposes as well.

As structural components of the cell, fats are extremely important for holding energy and allowing our cells to properly function.

This leads us to one of the major problems that results from consuming PUFA.

When we consume PUFA, they’re incorporated as structural components in our cells, including their mitochondria (18). But, the presence of double bonds in PUFA makes them weak, so they serve as extremely poor structural components.

As poor structural components, PUFA cause our cells, or more specifically our mitochondria, to leak energy! (19, 20, 21, 22, 23). And in addition to leaking energy, they also cause our cells to leak out ions like potassium (21).

When taken together, these two effects drastically increase our energy demands and reduce the efficiency of energy usage.

 

Polyunsaturated fats are converted into harmful, inflammatory compounds

When not used structurally, PUFA can be converted into various compounds, like the eicosanoids.

The eicosanoids are the major compounds responsible for inflammation in the body. These are the compounds that the various anti-inflammatory medications, like aspirin and ibuprofen, block.

Chronic inflammation is one of the primary markers of chronic disease, and this chronic inflammation requires PUFA. In other words, reducing PUFA consumption is a great way to reduce inflammation.

But, it doesn’t end there.

PUFA can be converted into many other compounds that directly inhibit energy production (24, 25, 26, 27) and contribute to stress (28, 29).

Again, these effects are disastrous for energy balance.

 

Polyunsaturated fats are highly susceptible to damage

The first 2 properties of PUFA have been predicated on the fats remaining intact. But, because of the double bonds in these fats, they’re extremely susceptible to damage through a process called lipid peroxidation (17).

And this damage wreaks havoc in our body.

The peroxidation of PUFA causes oxidative stress and inflammation throughout our cells, which directly inhibits energy production and even damages the DNA and protein structure of our cells (17, 30).

Because of this extensive damage, lipid peroxidation is considered to be a crucial step in the development of many chronic conditions (31).

 

Saturated fats to the rescue

Even individually, these 3 properties of PUFA make them incredibly harmful. And given all of them together, I would stay as far away from these fats as possible.

But this is easier said than done.

These fats are probably the biggest contributor to the health problems we’re seeing today, and they are EVERYWHERE!

They’re found in many baked goods, processed foods, cooking oils, fake butters & margarines, salad dressings, and fried foods. Plus, they’re encouraged as health foods in the form of nuts & seeds, fatty fish, and fatty chicken and pork.

But luckily, all the harmful properties of PUFA are directly contrasted by the saturated fats.

Saturated fats are everything PUFA are not. They’re stable, so they don’t leak energy and are extremely resistant to damage, and they aren’t converted to dangerous compounds. And, they even protect against the effects of PUFA! (32)

So, replacing PUFA with saturated (and monounsaturated) fats like butter and coconut oil will go a long way for improving energy balance.

While it might go without saying, reducing or avoiding PUFA might take a bit of work. But it’s well worth it if you care about your health.

 

References

Fats: We’ve Got It All Wrong

Somehow, the USDA still tells us not to consume more than 10% of our calories from saturated fat (1).

This is after they removed their recommendations to limit dietary cholesterol, and 4 years after TIME magazine declared that the war on fat had ended with a photo of butter on the cover and the mantra “Eat Butter” underneath.

In the TIME article they detailed how fat, specifically saturated fat, “has been the most vilified nutrient in the American diet” and that “our demonization of fat may have backfired in ways we are just beginning to understand.”

Yet, the battle against the evil, artery-clogging saturated fat rages on.

The article also explains the extremely flawed science that began the anti-saturated fat nonsense and details the lack of connection between saturated fat and heart disease. (Saturated fat has been blamed for heart disease because it raises LDL levels, although I explain the problems with this idea here.)

But while I agree with these points, if the TIME magazine article is any indication, we’re still completely lost when it comes to fats. The article shifts the blame to sugar, which I’ve already written several articles defending, and also touts the benefits of the polyunsaturated fats.

Herein lies an even bigger problem.

Not only are we still recommended to reduce our saturated fat consumption, we’re encouraged to replace these saturated fats with unsaturated fat, specifically the polyunsaturated fats.

 

What Are Polyunsaturated Fats?

While saturated fats are known as the heart-disease-causing fats, polyunsaturated fats are typically considered the “heart-healthy” fats.

Polyunsaturated fats, or PUFA, are the omega-3 and omega-6 fats that we’ve been encouraged to consume in place of the saturated fats. They’re found in fatty fish like salmon, nuts & seeds, and the vegetable oils that come from those nuts and seeds.

But, while the saturated fats have more or less been vindicated of their “artery-clogging” accusations, the general stance towards PUFA hasn’t changed. They’re still considered the angels of the fat world.

But, unlike the saturated fats, the polyunsaturated fats do contribute to heart disease (2, 3, 4, 5).

And they also contribute to virtually all other chronic conditions, including obesity & diabetes (6, 7), cancer (2, 8), fatty liver (9), and Alzheimer’s & Parkinson’s disease (10, 11, 12). This is not to mention that they’re also strongly immunosuppressive (13, 14, 15, 16).

So, how is it that these fats are so incredibly harmful?

Polyunsaturated fats have multiple double bonds in their carbon chains. This is what separates them from saturated fats, which don’t have any double bonds in their carbon chains.

The presence of double bonds in PUFA might sound like a minor detail, but it ends up causing problems at the most fundamental level of our health: energy balance.

Polyunsaturated fats inhibit energy production, drastically increase energy demands, and reduce the efficiency of energy usage.

These effects are so powerful that, beyond contributing to the chronic conditions I just mentioned, the PUFA content in our cells is also the primary determinant of lifespan and aging in all animals, including us humans! (17)

The reasons for these effects comes down to 3 properties of PUFA:

  • They’re structurally weak
  • They’re converted into harmful, inflammatory compounds
  • They’re highly susceptible to damage

Let’s explore each of these properties a little more.

 

Polyunsaturated fats are structurally weak

We often only consider the fats we eat as sources of energy. But, fats serve functional and structural purposes as well.

As structural components of the cell, fats are extremely important for holding energy and allowing our cells to properly function.

This leads us to one of the major problems that results from consuming PUFA.

When we consume PUFA, they’re incorporated as structural components in our cells, including their mitochondria (18). But, the presence of double bonds in PUFA makes them weak, so they serve as extremely poor structural components.

As poor structural components, PUFA cause our cells, or more specifically our mitochondria, to leak energy! (19, 20, 21, 22, 23). And in addition to leaking energy, they also cause our cells to leak out ions like potassium (21).

When taken together, these two effects drastically increase our energy demands and reduce the efficiency of energy usage.

 

Polyunsaturated fats are converted into harmful, inflammatory compounds

When not used structurally, PUFA can be converted into various compounds, like the eicosanoids.

The eicosanoids are the major compounds responsible for inflammation in the body. These are the compounds that the various anti-inflammatory medications, like aspirin and ibuprofen, block.

Chronic inflammation is one of the primary markers of chronic disease, and this chronic inflammation requires PUFA. In other words, reducing PUFA consumption is a great way to reduce inflammation.

But, it doesn’t end there.

PUFA can be converted into many other compounds that directly inhibit energy production (24, 25, 26, 27) and contribute to stress (28, 29).

Again, these effects are disastrous for energy balance.

 

Polyunsaturated fats are highly susceptible to damage

The first 2 properties of PUFA have been predicated on the fats remaining intact. But, because of the double bonds in these fats, they’re extremely susceptible to damage through a process called lipid peroxidation (17).

And this damage wreaks havoc in our body.

The peroxidation of PUFA causes oxidative stress and inflammation throughout our cells, which directly inhibits energy production and even damages the DNA and protein structure of our cells (17, 30).

Because of this extensive damage, lipid peroxidation is considered to be a crucial step in the development of many chronic conditions (31).

 

Saturated fats to the rescue

Even individually, these 3 properties of PUFA make them incredibly harmful. And given all of them together, I would stay as far away from these fats as possible.

But this is easier said than done.

These fats are probably the biggest contributor to the health problems we’re seeing today, and they are EVERYWHERE!

They’re found in many baked goods, processed foods, cooking oils, fake butters & margarines, salad dressings, and fried foods. Plus, they’re encouraged as health foods in the form of nuts & seeds, fatty fish, and fatty chicken and pork.

But luckily, all the harmful properties of PUFA are directly contrasted by the saturated fats.

Saturated fats are everything PUFA are not. They’re stable, so they don’t leak energy and are extremely resistant to damage, and they aren’t converted to dangerous compounds. And, they even protect against the effects of PUFA! (32)

So, replacing PUFA with saturated (and monounsaturated) fats like butter and coconut oil will go a long way for improving energy balance.

While it might go without saying, reducing or avoiding PUFA might take a bit of work. But it’s well worth it if you care about your health.

 

References

Fats: We’ve Got It All Wrong

Somehow, the USDA still tells us not to consume more than 10% of our calories from saturated fat (1).

This is after they removed their recommendations to limit dietary cholesterol, and 4 years after TIME magazine declared that the war on fat had ended with a photo of butter on the cover and the mantra “Eat Butter” underneath.

In the TIME article they detailed how fat, specifically saturated fat, “has been the most vilified nutrient in the American diet” and that “our demonization of fat may have backfired in ways we are just beginning to understand.”

Yet, the battle against the evil, artery-clogging saturated fat rages on.

The article also explains the extremely flawed science that began the anti-saturated fat nonsense and details the lack of connection between saturated fat and heart disease. (Saturated fat has been blamed for heart disease because it raises LDL levels, although I explain the problems with this idea here.)

But while I agree with these points, if the TIME magazine article is any indication, we’re still completely lost when it comes to fats. The article shifts the blame to sugar, which I’ve already written several articles defending, and also touts the benefits of the polyunsaturated fats.

Herein lies an even bigger problem.

Not only are we still recommended to reduce our saturated fat consumption, we’re encouraged to replace these saturated fats with unsaturated fat, specifically the polyunsaturated fats.

 

What Are Polyunsaturated Fats?

While saturated fats are known as the heart-disease-causing fats, polyunsaturated fats are typically considered the “heart-healthy” fats.

Polyunsaturated fats, or PUFA, are the omega-3 and omega-6 fats that we’ve been encouraged to consume in place of the saturated fats. They’re found in fatty fish like salmon, nuts & seeds, and the vegetable oils that come from those nuts and seeds.

But, while the saturated fats have more or less been vindicated of their “artery-clogging” accusations, the general stance towards PUFA hasn’t changed. They’re still considered the angels of the fat world.

But, unlike the saturated fats, the polyunsaturated fats do contribute to heart disease (2, 3, 4, 5).

And they also contribute to virtually all other chronic conditions, including obesity & diabetes (6, 7), cancer (2, 8), fatty liver (9), and Alzheimer’s & Parkinson’s disease (10, 11, 12). This is not to mention that they’re also strongly immunosuppressive (13, 14, 15, 16).

So, how is it that these fats are so incredibly harmful?

Polyunsaturated fats have multiple double bonds in their carbon chains. This is what separates them from saturated fats, which don’t have any double bonds in their carbon chains.

The presence of double bonds in PUFA might sound like a minor detail, but it ends up causing problems at the most fundamental level of our health: energy balance.

Polyunsaturated fats inhibit energy production, drastically increase energy demands, and reduce the efficiency of energy usage.

These effects are so powerful that, beyond contributing to the chronic conditions I just mentioned, the PUFA content in our cells is also the primary determinant of lifespan and aging in all animals, including us humans! (17)

The reasons for these effects comes down to 3 properties of PUFA:

  • They’re structurally weak
  • They’re converted into harmful, inflammatory compounds
  • They’re highly susceptible to damage

Let’s explore each of these properties a little more.

 

Polyunsaturated fats are structurally weak

We often only consider the fats we eat as sources of energy. But, fats serve functional and structural purposes as well.

As structural components of the cell, fats are extremely important for holding energy and allowing our cells to properly function.

This leads us to one of the major problems that results from consuming PUFA.

When we consume PUFA, they’re incorporated as structural components in our cells, including their mitochondria (18). But, the presence of double bonds in PUFA makes them weak, so they serve as extremely poor structural components.

As poor structural components, PUFA cause our cells, or more specifically our mitochondria, to leak energy! (19, 20, 21, 22, 23). And in addition to leaking energy, they also cause our cells to leak out ions like potassium (21).

When taken together, these two effects drastically increase our energy demands and reduce the efficiency of energy usage.

 

Polyunsaturated fats are converted into harmful, inflammatory compounds

When not used structurally, PUFA can be converted into various compounds, like the eicosanoids.

The eicosanoids are the major compounds responsible for inflammation in the body. These are the compounds that the various anti-inflammatory medications, like aspirin and ibuprofen, block.

Chronic inflammation is one of the primary markers of chronic disease, and this chronic inflammation requires PUFA. In other words, reducing PUFA consumption is a great way to reduce inflammation.

But, it doesn’t end there.

PUFA can be converted into many other compounds that directly inhibit energy production (24, 25, 26, 27) and contribute to stress (28, 29).

Again, these effects are disastrous for energy balance.

 

Polyunsaturated fats are highly susceptible to damage

The first 2 properties of PUFA have been predicated on the fats remaining intact. But, because of the double bonds in these fats, they’re extremely susceptible to damage through a process called lipid peroxidation (17).

And this damage wreaks havoc in our body.

The peroxidation of PUFA causes oxidative stress and inflammation throughout our cells, which directly inhibits energy production and even damages the DNA and protein structure of our cells (17, 30).

Because of this extensive damage, lipid peroxidation is considered to be a crucial step in the development of many chronic conditions (31).

 

Saturated fats to the rescue

Even individually, these 3 properties of PUFA make them incredibly harmful. And given all of them together, I would stay as far away from these fats as possible.

But this is easier said than done.

These fats are probably the biggest contributor to the health problems we’re seeing today, and they are EVERYWHERE!

They’re found in many baked goods, processed foods, cooking oils, fake butters & margarines, salad dressings, and fried foods. Plus, they’re encouraged as health foods in the form of nuts & seeds, fatty fish, and fatty chicken and pork.

But luckily, all the harmful properties of PUFA are directly contrasted by the saturated fats.

Saturated fats are everything PUFA are not. They’re stable, so they don’t leak energy and are extremely resistant to damage, and they aren’t converted to dangerous compounds. And, they even protect against the effects of PUFA! (32)

So, replacing PUFA with saturated (and monounsaturated) fats like butter and coconut oil will go a long way for improving energy balance.

While it might go without saying, reducing or avoiding PUFA might take a bit of work. But it’s well worth it if you care about your health.

 

References

Fats: We’ve Got It All Wrong

Somehow, the USDA still tells us not to consume more than 10% of our calories from saturated fat (1).

This is after they removed their recommendations to limit dietary cholesterol, and 4 years after TIME magazine declared that the war on fat had ended with a photo of butter on the cover and the mantra “Eat Butter” underneath.

In the TIME article they detailed how fat, specifically saturated fat, “has been the most vilified nutrient in the American diet” and that “our demonization of fat may have backfired in ways we are just beginning to understand.”

Yet, the battle against the evil, artery-clogging saturated fat rages on.

The article also explains the extremely flawed science that began the anti-saturated fat nonsense and details the lack of connection between saturated fat and heart disease. (Saturated fat has been blamed for heart disease because it raises LDL levels, although I explain the problems with this idea here.)

But while I agree with these points, if the TIME magazine article is any indication, we’re still completely lost when it comes to fats. The article shifts the blame to sugar, which I’ve already written several articles defending, and also touts the benefits of the polyunsaturated fats.

Herein lies an even bigger problem.

Not only are we still recommended to reduce our saturated fat consumption, we’re encouraged to replace these saturated fats with unsaturated fat, specifically the polyunsaturated fats.

 

What Are Polyunsaturated Fats?

While saturated fats are known as the heart-disease-causing fats, polyunsaturated fats are typically considered the “heart-healthy” fats.

Polyunsaturated fats, or PUFA, are the omega-3 and omega-6 fats that we’ve been encouraged to consume in place of the saturated fats. They’re found in fatty fish like salmon, nuts & seeds, and the vegetable oils that come from those nuts and seeds.

But, while the saturated fats have more or less been vindicated of their “artery-clogging” accusations, the general stance towards PUFA hasn’t changed. They’re still considered the angels of the fat world.

But, unlike the saturated fats, the polyunsaturated fats do contribute to heart disease (2, 3, 4, 5).

And they also contribute to virtually all other chronic conditions, including obesity & diabetes (6, 7), cancer (2, 8), fatty liver (9), and Alzheimer’s & Parkinson’s disease (10, 11, 12). This is not to mention that they’re also strongly immunosuppressive (13, 14, 15, 16).

So, how is it that these fats are so incredibly harmful?

Polyunsaturated fats have multiple double bonds in their carbon chains. This is what separates them from saturated fats, which don’t have any double bonds in their carbon chains.

The presence of double bonds in PUFA might sound like a minor detail, but it ends up causing problems at the most fundamental level of our health: energy balance.

Polyunsaturated fats inhibit energy production, drastically increase energy demands, and reduce the efficiency of energy usage.

These effects are so powerful that, beyond contributing to the chronic conditions I just mentioned, the PUFA content in our cells is also the primary determinant of lifespan and aging in all animals, including us humans! (17)

The reasons for these effects comes down to 3 properties of PUFA:

  • They’re structurally weak
  • They’re converted into harmful, inflammatory compounds
  • They’re highly susceptible to damage

Let’s explore each of these properties a little more.

 

Polyunsaturated fats are structurally weak

We often only consider the fats we eat as sources of energy. But, fats serve functional and structural purposes as well.

As structural components of the cell, fats are extremely important for holding energy and allowing our cells to properly function.

This leads us to one of the major problems that results from consuming PUFA.

When we consume PUFA, they’re incorporated as structural components in our cells, including their mitochondria (18). But, the presence of double bonds in PUFA makes them weak, so they serve as extremely poor structural components.

As poor structural components, PUFA cause our cells, or more specifically our mitochondria, to leak energy! (19, 20, 21, 22, 23). And in addition to leaking energy, they also cause our cells to leak out ions like potassium (21).

When taken together, these two effects drastically increase our energy demands and reduce the efficiency of energy usage.

 

Polyunsaturated fats are converted into harmful, inflammatory compounds

When not used structurally, PUFA can be converted into various compounds, like the eicosanoids.

The eicosanoids are the major compounds responsible for inflammation in the body. These are the compounds that the various anti-inflammatory medications, like aspirin and ibuprofen, block.

Chronic inflammation is one of the primary markers of chronic disease, and this chronic inflammation requires PUFA. In other words, reducing PUFA consumption is a great way to reduce inflammation.

But, it doesn’t end there.

PUFA can be converted into many other compounds that directly inhibit energy production (24, 25, 26, 27) and contribute to stress (28, 29).

Again, these effects are disastrous for energy balance.

 

Polyunsaturated fats are highly susceptible to damage

The first 2 properties of PUFA have been predicated on the fats remaining intact. But, because of the double bonds in these fats, they’re extremely susceptible to damage through a process called lipid peroxidation (17).

And this damage wreaks havoc in our body.

The peroxidation of PUFA causes oxidative stress and inflammation throughout our cells, which directly inhibits energy production and even damages the DNA and protein structure of our cells (17, 30).

Because of this extensive damage, lipid peroxidation is considered to be a crucial step in the development of many chronic conditions (31).

 

Saturated fats to the rescue

Even individually, these 3 properties of PUFA make them incredibly harmful. And given all of them together, I would stay as far away from these fats as possible.

But this is easier said than done.

These fats are probably the biggest contributor to the health problems we’re seeing today, and they are EVERYWHERE!

They’re found in many baked goods, processed foods, cooking oils, fake butters & margarines, salad dressings, and fried foods. Plus, they’re encouraged as health foods in the form of nuts & seeds, fatty fish, and fatty chicken and pork.

But luckily, all the harmful properties of PUFA are directly contrasted by the saturated fats.

Saturated fats are everything PUFA are not. They’re stable, so they don’t leak energy and are extremely resistant to damage, and they aren’t converted to dangerous compounds. And, they even protect against the effects of PUFA! (32)

So, replacing PUFA with saturated (and monounsaturated) fats like butter and coconut oil will go a long way for improving energy balance.

While it might go without saying, reducing or avoiding PUFA might take a bit of work. But it’s well worth it if you care about your health.

 

References

Fats: We’ve Got It All Wrong

Somehow, the USDA still tells us not to consume more than 10% of our calories from saturated fat (1).

This is after they removed their recommendations to limit dietary cholesterol, and 4 years after TIME magazine declared that the war on fat had ended with a photo of butter on the cover and the mantra “Eat Butter” underneath.

In the TIME article they detailed how fat, specifically saturated fat, “has been the most vilified nutrient in the American diet” and that “our demonization of fat may have backfired in ways we are just beginning to understand.”

Yet, the battle against the evil, artery-clogging saturated fat rages on.

The article also explains the extremely flawed science that began the anti-saturated fat nonsense and details the lack of connection between saturated fat and heart disease. (Saturated fat has been blamed for heart disease because it raises LDL levels, although I explain the problems with this idea here.)

But while I agree with these points, if the TIME magazine article is any indication, we’re still completely lost when it comes to fats. The article shifts the blame to sugar, which I’ve already written several articles defending, and also touts the benefits of the polyunsaturated fats.

Herein lies an even bigger problem.

Not only are we still recommended to reduce our saturated fat consumption, we’re encouraged to replace these saturated fats with unsaturated fat, specifically the polyunsaturated fats.

 

What Are Polyunsaturated Fats?

While saturated fats are known as the heart-disease-causing fats, polyunsaturated fats are typically considered the “heart-healthy” fats.

Polyunsaturated fats, or PUFA, are the omega-3 and omega-6 fats that we’ve been encouraged to consume in place of the saturated fats. They’re found in fatty fish like salmon, nuts & seeds, and the vegetable oils that come from those nuts and seeds.

But, while the saturated fats have more or less been vindicated of their “artery-clogging” accusations, the general stance towards PUFA hasn’t changed. They’re still considered the angels of the fat world.

But, unlike the saturated fats, the polyunsaturated fats do contribute to heart disease (2, 3, 4, 5).

And they also contribute to virtually all other chronic conditions, including obesity & diabetes (6, 7), cancer (2, 8), fatty liver (9), and Alzheimer’s & Parkinson’s disease (10, 11, 12). This is not to mention that they’re also strongly immunosuppressive (13, 14, 15, 16).

So, how is it that these fats are so incredibly harmful?

Polyunsaturated fats have multiple double bonds in their carbon chains. This is what separates them from saturated fats, which don’t have any double bonds in their carbon chains.

The presence of double bonds in PUFA might sound like a minor detail, but it ends up causing problems at the most fundamental level of our health: energy balance.

Polyunsaturated fats inhibit energy production, drastically increase energy demands, and reduce the efficiency of energy usage.

These effects are so powerful that, beyond contributing to the chronic conditions I just mentioned, the PUFA content in our cells is also the primary determinant of lifespan and aging in all animals, including us humans! (17)

The reasons for these effects comes down to 3 properties of PUFA:

  • They’re structurally weak
  • They’re converted into harmful, inflammatory compounds
  • They’re highly susceptible to damage

Let’s explore each of these properties a little more.

 

Polyunsaturated fats are structurally weak

We often only consider the fats we eat as sources of energy. But, fats serve functional and structural purposes as well.

As structural components of the cell, fats are extremely important for holding energy and allowing our cells to properly function.

This leads us to one of the major problems that results from consuming PUFA.

When we consume PUFA, they’re incorporated as structural components in our cells, including their mitochondria (18). But, the presence of double bonds in PUFA makes them weak, so they serve as extremely poor structural components.

As poor structural components, PUFA cause our cells, or more specifically our mitochondria, to leak energy! (19, 20, 21, 22, 23). And in addition to leaking energy, they also cause our cells to leak out ions like potassium (21).

When taken together, these two effects drastically increase our energy demands and reduce the efficiency of energy usage.

 

Polyunsaturated fats are converted into harmful, inflammatory compounds

When not used structurally, PUFA can be converted into various compounds, like the eicosanoids.

The eicosanoids are the major compounds responsible for inflammation in the body. These are the compounds that the various anti-inflammatory medications, like aspirin and ibuprofen, block.

Chronic inflammation is one of the primary markers of chronic disease, and this chronic inflammation requires PUFA. In other words, reducing PUFA consumption is a great way to reduce inflammation.

But, it doesn’t end there.

PUFA can be converted into many other compounds that directly inhibit energy production (24, 25, 26, 27) and contribute to stress (28, 29).

Again, these effects are disastrous for energy balance.

 

Polyunsaturated fats are highly susceptible to damage

The first 2 properties of PUFA have been predicated on the fats remaining intact. But, because of the double bonds in these fats, they’re extremely susceptible to damage through a process called lipid peroxidation (17).

And this damage wreaks havoc in our body.

The peroxidation of PUFA causes oxidative stress and inflammation throughout our cells, which directly inhibits energy production and even damages the DNA and protein structure of our cells (17, 30).

Because of this extensive damage, lipid peroxidation is considered to be a crucial step in the development of many chronic conditions (31).

 

Saturated fats to the rescue

Even individually, these 3 properties of PUFA make them incredibly harmful. And given all of them together, I would stay as far away from these fats as possible.

But this is easier said than done.

These fats are probably the biggest contributor to the health problems we’re seeing today, and they are EVERYWHERE!

They’re found in many baked goods, processed foods, cooking oils, fake butters & margarines, salad dressings, and fried foods. Plus, they’re encouraged as health foods in the form of nuts & seeds, fatty fish, and fatty chicken and pork.

But luckily, all the harmful properties of PUFA are directly contrasted by the saturated fats.

Saturated fats are everything PUFA are not. They’re stable, so they don’t leak energy and are extremely resistant to damage, and they aren’t converted to dangerous compounds. And, they even protect against the effects of PUFA! (32)

So, replacing PUFA with saturated (and monounsaturated) fats like butter and coconut oil will go a long way for improving energy balance.

While it might go without saying, reducing or avoiding PUFA might take a bit of work. But it’s well worth it if you care about your health.

 

References

Fats: We’ve Got It All Wrong

Somehow, the USDA still tells us not to consume more than 10% of our calories from saturated fat (1).

This is after they removed their recommendations to limit dietary cholesterol, and 4 years after TIME magazine declared that the war on fat had ended with a photo of butter on the cover and the mantra “Eat Butter” underneath.

In the TIME article they detailed how fat, specifically saturated fat, “has been the most vilified nutrient in the American diet” and that “our demonization of fat may have backfired in ways we are just beginning to understand.”

Yet, the battle against the evil, artery-clogging saturated fat rages on.

The article also explains the extremely flawed science that began the anti-saturated fat nonsense and details the lack of connection between saturated fat and heart disease. (Saturated fat has been blamed for heart disease because it raises LDL levels, although I explain the problems with this idea here.)

But while I agree with these points, if the TIME magazine article is any indication, we’re still completely lost when it comes to fats. The article shifts the blame to sugar, which I’ve already written several articles defending, and also touts the benefits of the polyunsaturated fats.

Herein lies an even bigger problem.

Not only are we still recommended to reduce our saturated fat consumption, we’re encouraged to replace these saturated fats with unsaturated fat, specifically the polyunsaturated fats.

 

What Are Polyunsaturated Fats?

While saturated fats are known as the heart-disease-causing fats, polyunsaturated fats are typically considered the “heart-healthy” fats.

Polyunsaturated fats, or PUFA, are the omega-3 and omega-6 fats that we’ve been encouraged to consume in place of the saturated fats. They’re found in fatty fish like salmon, nuts & seeds, and the vegetable oils that come from those nuts and seeds.

But, while the saturated fats have more or less been vindicated of their “artery-clogging” accusations, the general stance towards PUFA hasn’t changed. They’re still considered the angels of the fat world.

But, unlike the saturated fats, the polyunsaturated fats do contribute to heart disease (2, 3, 4, 5).

And they also contribute to virtually all other chronic conditions, including obesity & diabetes (6, 7), cancer (2, 8), fatty liver (9), and Alzheimer’s & Parkinson’s disease (10, 11, 12). This is not to mention that they’re also strongly immunosuppressive (13, 14, 15, 16).

So, how is it that these fats are so incredibly harmful?

Polyunsaturated fats have multiple double bonds in their carbon chains. This is what separates them from saturated fats, which don’t have any double bonds in their carbon chains.

The presence of double bonds in PUFA might sound like a minor detail, but it ends up causing problems at the most fundamental level of our health: energy balance.

Polyunsaturated fats inhibit energy production, drastically increase energy demands, and reduce the efficiency of energy usage.

These effects are so powerful that, beyond contributing to the chronic conditions I just mentioned, the PUFA content in our cells is also the primary determinant of lifespan and aging in all animals, including us humans! (17)

The reasons for these effects comes down to 3 properties of PUFA:

  • They’re structurally weak
  • They’re converted into harmful, inflammatory compounds
  • They’re highly susceptible to damage

Let’s explore each of these properties a little more.

 

Polyunsaturated fats are structurally weak

We often only consider the fats we eat as sources of energy. But, fats serve functional and structural purposes as well.

As structural components of the cell, fats are extremely important for holding energy and allowing our cells to properly function.

This leads us to one of the major problems that results from consuming PUFA.

When we consume PUFA, they’re incorporated as structural components in our cells, including their mitochondria (18). But, the presence of double bonds in PUFA makes them weak, so they serve as extremely poor structural components.

As poor structural components, PUFA cause our cells, or more specifically our mitochondria, to leak energy! (19, 20, 21, 22, 23). And in addition to leaking energy, they also cause our cells to leak out ions like potassium (21).

When taken together, these two effects drastically increase our energy demands and reduce the efficiency of energy usage.

 

Polyunsaturated fats are converted into harmful, inflammatory compounds

When not used structurally, PUFA can be converted into various compounds, like the eicosanoids.

The eicosanoids are the major compounds responsible for inflammation in the body. These are the compounds that the various anti-inflammatory medications, like aspirin and ibuprofen, block.

Chronic inflammation is one of the primary markers of chronic disease, and this chronic inflammation requires PUFA. In other words, reducing PUFA consumption is a great way to reduce inflammation.

But, it doesn’t end there.

PUFA can be converted into many other compounds that directly inhibit energy production (24, 25, 26, 27) and contribute to stress (28, 29).

Again, these effects are disastrous for energy balance.

 

Polyunsaturated fats are highly susceptible to damage

The first 2 properties of PUFA have been predicated on the fats remaining intact. But, because of the double bonds in these fats, they’re extremely susceptible to damage through a process called lipid peroxidation (17).

And this damage wreaks havoc in our body.

The peroxidation of PUFA causes oxidative stress and inflammation throughout our cells, which directly inhibits energy production and even damages the DNA and protein structure of our cells (17, 30).

Because of this extensive damage, lipid peroxidation is considered to be a crucial step in the development of many chronic conditions (31).

 

Saturated fats to the rescue

Even individually, these 3 properties of PUFA make them incredibly harmful. And given all of them together, I would stay as far away from these fats as possible.

But this is easier said than done.

These fats are probably the biggest contributor to the health problems we’re seeing today, and they are EVERYWHERE!

They’re found in many baked goods, processed foods, cooking oils, fake butters & margarines, salad dressings, and fried foods. Plus, they’re encouraged as health foods in the form of nuts & seeds, fatty fish, and fatty chicken and pork.

But luckily, all the harmful properties of PUFA are directly contrasted by the saturated fats.

Saturated fats are everything PUFA are not. They’re stable, so they don’t leak energy and are extremely resistant to damage, and they aren’t converted to dangerous compounds. And, they even protect against the effects of PUFA! (32)

So, replacing PUFA with saturated (and monounsaturated) fats like butter and coconut oil will go a long way for improving energy balance.

While it might go without saying, reducing or avoiding PUFA might take a bit of work. But it’s well worth it if you care about your health.

 

References

Fats: We’ve Got It All Wrong

Somehow, the USDA still tells us not to consume more than 10% of our calories from saturated fat (1).

This is after they removed their recommendations to limit dietary cholesterol, and 4 years after TIME magazine declared that the war on fat had ended with a photo of butter on the cover and the mantra “Eat Butter” underneath.

In the TIME article they detailed how fat, specifically saturated fat, “has been the most vilified nutrient in the American diet” and that “our demonization of fat may have backfired in ways we are just beginning to understand.”

Yet, the battle against the evil, artery-clogging saturated fat rages on.

The article also explains the extremely flawed science that began the anti-saturated fat nonsense and details the lack of connection between saturated fat and heart disease. (Saturated fat has been blamed for heart disease because it raises LDL levels, although I explain the problems with this idea here.)

But while I agree with these points, if the TIME magazine article is any indication, we’re still completely lost when it comes to fats. The article shifts the blame to sugar, which I’ve already written several articles defending, and also touts the benefits of the polyunsaturated fats.

Herein lies an even bigger problem.

Not only are we still recommended to reduce our saturated fat consumption, we’re encouraged to replace these saturated fats with unsaturated fat, specifically the polyunsaturated fats.

 

What Are Polyunsaturated Fats?

While saturated fats are known as the heart-disease-causing fats, polyunsaturated fats are typically considered the “heart-healthy” fats.

Polyunsaturated fats, or PUFA, are the omega-3 and omega-6 fats that we’ve been encouraged to consume in place of the saturated fats. They’re found in fatty fish like salmon, nuts & seeds, and the vegetable oils that come from those nuts and seeds.

But, while the saturated fats have more or less been vindicated of their “artery-clogging” accusations, the general stance towards PUFA hasn’t changed. They’re still considered the angels of the fat world.

But, unlike the saturated fats, the polyunsaturated fats do contribute to heart disease (2, 3, 4, 5).

And they also contribute to virtually all other chronic conditions, including obesity & diabetes (6, 7), cancer (2, 8), fatty liver (9), and Alzheimer’s & Parkinson’s disease (10, 11, 12). This is not to mention that they’re also strongly immunosuppressive (13, 14, 15, 16).

So, how is it that these fats are so incredibly harmful?

Polyunsaturated fats have multiple double bonds in their carbon chains. This is what separates them from saturated fats, which don’t have any double bonds in their carbon chains.

The presence of double bonds in PUFA might sound like a minor detail, but it ends up causing problems at the most fundamental level of our health: energy balance.

Polyunsaturated fats inhibit energy production, drastically increase energy demands, and reduce the efficiency of energy usage.

These effects are so powerful that, beyond contributing to the chronic conditions I just mentioned, the PUFA content in our cells is also the primary determinant of lifespan and aging in all animals, including us humans! (17)

The reasons for these effects comes down to 3 properties of PUFA:

  • They’re structurally weak
  • They’re converted into harmful, inflammatory compounds
  • They’re highly susceptible to damage

Let’s explore each of these properties a little more.

 

Polyunsaturated fats are structurally weak

We often only consider the fats we eat as sources of energy. But, fats serve functional and structural purposes as well.

As structural components of the cell, fats are extremely important for holding energy and allowing our cells to properly function.

This leads us to one of the major problems that results from consuming PUFA.

When we consume PUFA, they’re incorporated as structural components in our cells, including their mitochondria (18). But, the presence of double bonds in PUFA makes them weak, so they serve as extremely poor structural components.

As poor structural components, PUFA cause our cells, or more specifically our mitochondria, to leak energy! (19, 20, 21, 22, 23). And in addition to leaking energy, they also cause our cells to leak out ions like potassium (21).

When taken together, these two effects drastically increase our energy demands and reduce the efficiency of energy usage.

 

Polyunsaturated fats are converted into harmful, inflammatory compounds

When not used structurally, PUFA can be converted into various compounds, like the eicosanoids.

The eicosanoids are the major compounds responsible for inflammation in the body. These are the compounds that the various anti-inflammatory medications, like aspirin and ibuprofen, block.

Chronic inflammation is one of the primary markers of chronic disease, and this chronic inflammation requires PUFA. In other words, reducing PUFA consumption is a great way to reduce inflammation.

But, it doesn’t end there.

PUFA can be converted into many other compounds that directly inhibit energy production (24, 25, 26, 27) and contribute to stress (28, 29).

Again, these effects are disastrous for energy balance.

 

Polyunsaturated fats are highly susceptible to damage

The first 2 properties of PUFA have been predicated on the fats remaining intact. But, because of the double bonds in these fats, they’re extremely susceptible to damage through a process called lipid peroxidation (17).

And this damage wreaks havoc in our body.

The peroxidation of PUFA causes oxidative stress and inflammation throughout our cells, which directly inhibits energy production and even damages the DNA and protein structure of our cells (17, 30).

Because of this extensive damage, lipid peroxidation is considered to be a crucial step in the development of many chronic conditions (31).

 

Saturated fats to the rescue

Even individually, these 3 properties of PUFA make them incredibly harmful. And given all of them together, I would stay as far away from these fats as possible.

But this is easier said than done.

These fats are probably the biggest contributor to the health problems we’re seeing today, and they are EVERYWHERE!

They’re found in many baked goods, processed foods, cooking oils, fake butters & margarines, salad dressings, and fried foods. Plus, they’re encouraged as health foods in the form of nuts & seeds, fatty fish, and fatty chicken and pork.

But luckily, all the harmful properties of PUFA are directly contrasted by the saturated fats.

Saturated fats are everything PUFA are not. They’re stable, so they don’t leak energy and are extremely resistant to damage, and they aren’t converted to dangerous compounds. And, they even protect against the effects of PUFA! (32)

So, replacing PUFA with saturated (and monounsaturated) fats like butter and coconut oil will go a long way for improving energy balance.

While it might go without saying, reducing or avoiding PUFA might take a bit of work. But it’s well worth it if you care about your health.

 

References

Fats: We’ve Got It All Wrong

Somehow, the USDA still tells us not to consume more than 10% of our calories from saturated fat (1).

This is after they removed their recommendations to limit dietary cholesterol, and 4 years after TIME magazine declared that the war on fat had ended with a photo of butter on the cover and the mantra “Eat Butter” underneath.

In the TIME article they detailed how fat, specifically saturated fat, “has been the most vilified nutrient in the American diet” and that “our demonization of fat may have backfired in ways we are just beginning to understand.”

Yet, the battle against the evil, artery-clogging saturated fat rages on.

The article also explains the extremely flawed science that began the anti-saturated fat nonsense and details the lack of connection between saturated fat and heart disease. (Saturated fat has been blamed for heart disease because it raises LDL levels, although I explain the problems with this idea here.)

But while I agree with these points, if the TIME magazine article is any indication, we’re still completely lost when it comes to fats. The article shifts the blame to sugar, which I’ve already written several articles defending, and also touts the benefits of the polyunsaturated fats.

Herein lies an even bigger problem.

Not only are we still recommended to reduce our saturated fat consumption, we’re encouraged to replace these saturated fats with unsaturated fat, specifically the polyunsaturated fats.

 

What Are Polyunsaturated Fats?

While saturated fats are known as the heart-disease-causing fats, polyunsaturated fats are typically considered the “heart-healthy” fats.

Polyunsaturated fats, or PUFA, are the omega-3 and omega-6 fats that we’ve been encouraged to consume in place of the saturated fats. They’re found in fatty fish like salmon, nuts & seeds, and the vegetable oils that come from those nuts and seeds.

But, while the saturated fats have more or less been vindicated of their “artery-clogging” accusations, the general stance towards PUFA hasn’t changed. They’re still considered the angels of the fat world.

But, unlike the saturated fats, the polyunsaturated fats do contribute to heart disease (2, 3, 4, 5).

And they also contribute to virtually all other chronic conditions, including obesity & diabetes (6, 7), cancer (2, 8), fatty liver (9), and Alzheimer’s & Parkinson’s disease (10, 11, 12). This is not to mention that they’re also strongly immunosuppressive (13, 14, 15, 16).

So, how is it that these fats are so incredibly harmful?

Polyunsaturated fats have multiple double bonds in their carbon chains. This is what separates them from saturated fats, which don’t have any double bonds in their carbon chains.

The presence of double bonds in PUFA might sound like a minor detail, but it ends up causing problems at the most fundamental level of our health: energy balance.

Polyunsaturated fats inhibit energy production, drastically increase energy demands, and reduce the efficiency of energy usage.

These effects are so powerful that, beyond contributing to the chronic conditions I just mentioned, the PUFA content in our cells is also the primary determinant of lifespan and aging in all animals, including us humans! (17)

The reasons for these effects comes down to 3 properties of PUFA:

  • They’re structurally weak
  • They’re converted into harmful, inflammatory compounds
  • They’re highly susceptible to damage

Let’s explore each of these properties a little more.

 

Polyunsaturated fats are structurally weak

We often only consider the fats we eat as sources of energy. But, fats serve functional and structural purposes as well.

As structural components of the cell, fats are extremely important for holding energy and allowing our cells to properly function.

This leads us to one of the major problems that results from consuming PUFA.

When we consume PUFA, they’re incorporated as structural components in our cells, including their mitochondria (18). But, the presence of double bonds in PUFA makes them weak, so they serve as extremely poor structural components.

As poor structural components, PUFA cause our cells, or more specifically our mitochondria, to leak energy! (19, 20, 21, 22, 23). And in addition to leaking energy, they also cause our cells to leak out ions like potassium (21).

When taken together, these two effects drastically increase our energy demands and reduce the efficiency of energy usage.

 

Polyunsaturated fats are converted into harmful, inflammatory compounds

When not used structurally, PUFA can be converted into various compounds, like the eicosanoids.

The eicosanoids are the major compounds responsible for inflammation in the body. These are the compounds that the various anti-inflammatory medications, like aspirin and ibuprofen, block.

Chronic inflammation is one of the primary markers of chronic disease, and this chronic inflammation requires PUFA. In other words, reducing PUFA consumption is a great way to reduce inflammation.

But, it doesn’t end there.

PUFA can be converted into many other compounds that directly inhibit energy production (24, 25, 26, 27) and contribute to stress (28, 29).

Again, these effects are disastrous for energy balance.

 

Polyunsaturated fats are highly susceptible to damage

The first 2 properties of PUFA have been predicated on the fats remaining intact. But, because of the double bonds in these fats, they’re extremely susceptible to damage through a process called lipid peroxidation (17).

And this damage wreaks havoc in our body.

The peroxidation of PUFA causes oxidative stress and inflammation throughout our cells, which directly inhibits energy production and even damages the DNA and protein structure of our cells (17, 30).

Because of this extensive damage, lipid peroxidation is considered to be a crucial step in the development of many chronic conditions (31).

 

Saturated fats to the rescue

Even individually, these 3 properties of PUFA make them incredibly harmful. And given all of them together, I would stay as far away from these fats as possible.

But this is easier said than done.

These fats are probably the biggest contributor to the health problems we’re seeing today, and they are EVERYWHERE!

They’re found in many baked goods, processed foods, cooking oils, fake butters & margarines, salad dressings, and fried foods. Plus, they’re encouraged as health foods in the form of nuts & seeds, fatty fish, and fatty chicken and pork.

But luckily, all the harmful properties of PUFA are directly contrasted by the saturated fats.

Saturated fats are everything PUFA are not. They’re stable, so they don’t leak energy and are extremely resistant to damage, and they aren’t converted to dangerous compounds. And, they even protect against the effects of PUFA! (32)

So, replacing PUFA with saturated (and monounsaturated) fats like butter and coconut oil will go a long way for improving energy balance.

While it might go without saying, reducing or avoiding PUFA might take a bit of work. But it’s well worth it if you care about your health.

 

References

Fats: We’ve Got It All Wrong

Somehow, the USDA still tells us not to consume more than 10% of our calories from saturated fat (1).

This is after they removed their recommendations to limit dietary cholesterol, and 4 years after TIME magazine declared that the war on fat had ended with a photo of butter on the cover and the mantra “Eat Butter” underneath.

In the TIME article they detailed how fat, specifically saturated fat, “has been the most vilified nutrient in the American diet” and that “our demonization of fat may have backfired in ways we are just beginning to understand.”

Yet, the battle against the evil, artery-clogging saturated fat rages on.

The article also explains the extremely flawed science that began the anti-saturated fat nonsense and details the lack of connection between saturated fat and heart disease. (Saturated fat has been blamed for heart disease because it raises LDL levels, although I explain the problems with this idea here.)

But while I agree with these points, if the TIME magazine article is any indication, we’re still completely lost when it comes to fats. The article shifts the blame to sugar, which I’ve already written several articles defending, and also touts the benefits of the polyunsaturated fats.

Herein lies an even bigger problem.

Not only are we still recommended to reduce our saturated fat consumption, we’re encouraged to replace these saturated fats with unsaturated fat, specifically the polyunsaturated fats.

 

What Are Polyunsaturated Fats?

While saturated fats are known as the heart-disease-causing fats, polyunsaturated fats are typically considered the “heart-healthy” fats.

Polyunsaturated fats, or PUFA, are the omega-3 and omega-6 fats that we’ve been encouraged to consume in place of the saturated fats. They’re found in fatty fish like salmon, nuts & seeds, and the vegetable oils that come from those nuts and seeds.

But, while the saturated fats have more or less been vindicated of their “artery-clogging” accusations, the general stance towards PUFA hasn’t changed. They’re still considered the angels of the fat world.

But, unlike the saturated fats, the polyunsaturated fats do contribute to heart disease (2, 3, 4, 5).

And they also contribute to virtually all other chronic conditions, including obesity & diabetes (6, 7), cancer (2, 8), fatty liver (9), and Alzheimer’s & Parkinson’s disease (10, 11, 12). This is not to mention that they’re also strongly immunosuppressive (13, 14, 15, 16).

So, how is it that these fats are so incredibly harmful?

Polyunsaturated fats have multiple double bonds in their carbon chains. This is what separates them from saturated fats, which don’t have any double bonds in their carbon chains.

The presence of double bonds in PUFA might sound like a minor detail, but it ends up causing problems at the most fundamental level of our health: energy balance.

Polyunsaturated fats inhibit energy production, drastically increase energy demands, and reduce the efficiency of energy usage.

These effects are so powerful that, beyond contributing to the chronic conditions I just mentioned, the PUFA content in our cells is also the primary determinant of lifespan and aging in all animals, including us humans! (17)

The reasons for these effects comes down to 3 properties of PUFA:

  • They’re structurally weak
  • They’re converted into harmful, inflammatory compounds
  • They’re highly susceptible to damage

Let’s explore each of these properties a little more.

 

Polyunsaturated fats are structurally weak

We often only consider the fats we eat as sources of energy. But, fats serve functional and structural purposes as well.

As structural components of the cell, fats are extremely important for holding energy and allowing our cells to properly function.

This leads us to one of the major problems that results from consuming PUFA.

When we consume PUFA, they’re incorporated as structural components in our cells, including their mitochondria (18). But, the presence of double bonds in PUFA makes them weak, so they serve as extremely poor structural components.

As poor structural components, PUFA cause our cells, or more specifically our mitochondria, to leak energy! (19, 20, 21, 22, 23). And in addition to leaking energy, they also cause our cells to leak out ions like potassium (21).

When taken together, these two effects drastically increase our energy demands and reduce the efficiency of energy usage.

 

Polyunsaturated fats are converted into harmful, inflammatory compounds

When not used structurally, PUFA can be converted into various compounds, like the eicosanoids.

The eicosanoids are the major compounds responsible for inflammation in the body. These are the compounds that the various anti-inflammatory medications, like aspirin and ibuprofen, block.

Chronic inflammation is one of the primary markers of chronic disease, and this chronic inflammation requires PUFA. In other words, reducing PUFA consumption is a great way to reduce inflammation.

But, it doesn’t end there.

PUFA can be converted into many other compounds that directly inhibit energy production (24, 25, 26, 27) and contribute to stress (28, 29).

Again, these effects are disastrous for energy balance.

 

Polyunsaturated fats are highly susceptible to damage

The first 2 properties of PUFA have been predicated on the fats remaining intact. But, because of the double bonds in these fats, they’re extremely susceptible to damage through a process called lipid peroxidation (17).

And this damage wreaks havoc in our body.

The peroxidation of PUFA causes oxidative stress and inflammation throughout our cells, which directly inhibits energy production and even damages the DNA and protein structure of our cells (17, 30).

Because of this extensive damage, lipid peroxidation is considered to be a crucial step in the development of many chronic conditions (31).

 

Saturated fats to the rescue

Even individually, these 3 properties of PUFA make them incredibly harmful. And given all of them together, I would stay as far away from these fats as possible.

But this is easier said than done.

These fats are probably the biggest contributor to the health problems we’re seeing today, and they are EVERYWHERE!

They’re found in many baked goods, processed foods, cooking oils, fake butters & margarines, salad dressings, and fried foods. Plus, they’re encouraged as health foods in the form of nuts & seeds, fatty fish, and fatty chicken and pork.

But luckily, all the harmful properties of PUFA are directly contrasted by the saturated fats.

Saturated fats are everything PUFA are not. They’re stable, so they don’t leak energy and are extremely resistant to damage, and they aren’t converted to dangerous compounds. And, they even protect against the effects of PUFA! (32)

So, replacing PUFA with saturated (and monounsaturated) fats like butter and coconut oil will go a long way for improving energy balance.

While it might go without saying, reducing or avoiding PUFA might take a bit of work. But it’s well worth it if you care about your health.

 

References

Fats: We’ve Got It All Wrong

Somehow, the USDA still tells us not to consume more than 10% of our calories from saturated fat (1).

This is after they removed their recommendations to limit dietary cholesterol, and 4 years after TIME magazine declared that the war on fat had ended with a photo of butter on the cover and the mantra “Eat Butter” underneath.

In the TIME article they detailed how fat, specifically saturated fat, “has been the most vilified nutrient in the American diet” and that “our demonization of fat may have backfired in ways we are just beginning to understand.”

Yet, the battle against the evil, artery-clogging saturated fat rages on.

The article also explains the extremely flawed science that began the anti-saturated fat nonsense and details the lack of connection between saturated fat and heart disease. (Saturated fat has been blamed for heart disease because it raises LDL levels, although I explain the problems with this idea here.)

But while I agree with these points, if the TIME magazine article is any indication, we’re still completely lost when it comes to fats. The article shifts the blame to sugar, which I’ve already written several articles defending, and also touts the benefits of the polyunsaturated fats.

Herein lies an even bigger problem.

Not only are we still recommended to reduce our saturated fat consumption, we’re encouraged to replace these saturated fats with unsaturated fat, specifically the polyunsaturated fats.

 

What Are Polyunsaturated Fats?

While saturated fats are known as the heart-disease-causing fats, polyunsaturated fats are typically considered the “heart-healthy” fats.

Polyunsaturated fats, or PUFA, are the omega-3 and omega-6 fats that we’ve been encouraged to consume in place of the saturated fats. They’re found in fatty fish like salmon, nuts & seeds, and the vegetable oils that come from those nuts and seeds.

But, while the saturated fats have more or less been vindicated of their “artery-clogging” accusations, the general stance towards PUFA hasn’t changed. They’re still considered the angels of the fat world.

But, unlike the saturated fats, the polyunsaturated fats do contribute to heart disease (2, 3, 4, 5).

And they also contribute to virtually all other chronic conditions, including obesity & diabetes (6, 7), cancer (2, 8), fatty liver (9), and Alzheimer’s & Parkinson’s disease (10, 11, 12). This is not to mention that they’re also strongly immunosuppressive (13, 14, 15, 16).

So, how is it that these fats are so incredibly harmful?

Polyunsaturated fats have multiple double bonds in their carbon chains. This is what separates them from saturated fats, which don’t have any double bonds in their carbon chains.

The presence of double bonds in PUFA might sound like a minor detail, but it ends up causing problems at the most fundamental level of our health: energy balance.

Polyunsaturated fats inhibit energy production, drastically increase energy demands, and reduce the efficiency of energy usage.

These effects are so powerful that, beyond contributing to the chronic conditions I just mentioned, the PUFA content in our cells is also the primary determinant of lifespan and aging in all animals, including us humans! (17)

The reasons for these effects comes down to 3 properties of PUFA:

  • They’re structurally weak
  • They’re converted into harmful, inflammatory compounds
  • They’re highly susceptible to damage

Let’s explore each of these properties a little more.

 

Polyunsaturated fats are structurally weak

We often only consider the fats we eat as sources of energy. But, fats serve functional and structural purposes as well.

As structural components of the cell, fats are extremely important for holding energy and allowing our cells to properly function.

This leads us to one of the major problems that results from consuming PUFA.

When we consume PUFA, they’re incorporated as structural components in our cells, including their mitochondria (18). But, the presence of double bonds in PUFA makes them weak, so they serve as extremely poor structural components.

As poor structural components, PUFA cause our cells, or more specifically our mitochondria, to leak energy! (19, 20, 21, 22, 23). And in addition to leaking energy, they also cause our cells to leak out ions like potassium (21).

When taken together, these two effects drastically increase our energy demands and reduce the efficiency of energy usage.

 

Polyunsaturated fats are converted into harmful, inflammatory compounds

When not used structurally, PUFA can be converted into various compounds, like the eicosanoids.

The eicosanoids are the major compounds responsible for inflammation in the body. These are the compounds that the various anti-inflammatory medications, like aspirin and ibuprofen, block.

Chronic inflammation is one of the primary markers of chronic disease, and this chronic inflammation requires PUFA. In other words, reducing PUFA consumption is a great way to reduce inflammation.

But, it doesn’t end there.

PUFA can be converted into many other compounds that directly inhibit energy production (24, 25, 26, 27) and contribute to stress (28, 29).

Again, these effects are disastrous for energy balance.

 

Polyunsaturated fats are highly susceptible to damage

The first 2 properties of PUFA have been predicated on the fats remaining intact. But, because of the double bonds in these fats, they’re extremely susceptible to damage through a process called lipid peroxidation (17).

And this damage wreaks havoc in our body.

The peroxidation of PUFA causes oxidative stress and inflammation throughout our cells, which directly inhibits energy production and even damages the DNA and protein structure of our cells (17, 30).

Because of this extensive damage, lipid peroxidation is considered to be a crucial step in the development of many chronic conditions (31).

 

Saturated fats to the rescue

Even individually, these 3 properties of PUFA make them incredibly harmful. And given all of them together, I would stay as far away from these fats as possible.

But this is easier said than done.

These fats are probably the biggest contributor to the health problems we’re seeing today, and they are EVERYWHERE!

They’re found in many baked goods, processed foods, cooking oils, fake butters & margarines, salad dressings, and fried foods. Plus, they’re encouraged as health foods in the form of nuts & seeds, fatty fish, and fatty chicken and pork.

But luckily, all the harmful properties of PUFA are directly contrasted by the saturated fats.

Saturated fats are everything PUFA are not. They’re stable, so they don’t leak energy and are extremely resistant to damage, and they aren’t converted to dangerous compounds. And, they even protect against the effects of PUFA! (32)

So, replacing PUFA with saturated (and monounsaturated) fats like butter and coconut oil will go a long way for improving energy balance.

While it might go without saying, reducing or avoiding PUFA might take a bit of work. But it’s well worth it if you care about your health.

 

References

Sugar Does NOT Cause Insulin Resistance or Diabetes

Insulin resistance is one of the main components of metabolic syndrome, which increases heart disease risk, diabetes risk, and overall mortality (1).

Diabetes and prediabetes, which are considered to be a result of insulin resistance, have reached epidemic levels. 114 million U.S. adults have diabetes or prediabetes, accounting for a staggering 35% of the entire U.S. population! (2) And the numbers are only increasing.

The worst part is that the current recommendations for handling insulin resistance and diabetes only make them worse. These recommendations center around the mistaken belief that the consumption of carbohydrates, specifically sugar, is to blame for causing and worsening these conditions.

This is a huge problem, to say the least.

What are Insulin Resistance and Diabetes?

Insulin is one of the regulators of our blood sugar.

When we consume any form of carbohydrates, including sugars, our blood sugar increases. The increase in blood sugar triggers the release of insulin, which allows sugar to move from the blood into the cells where it can be used to produce energy.

The conventional view of insulin resistance is that the cells don’t respond as well to insulin (they “resist” insulin’s effects), so the sugar isn’t moved from the blood into the cells, causing blood sugar levels to remain slightly elevated. Diabetes (type 2) is considered to be the result of a more intense form of insulin resistance, where the cells respond even less to insulin and blood sugar levels remain very high.

From this view, the problem in insulin resistance and diabetes is that sugar can’t be transported into the cells where it’s needed. But, as you’ll read in a little bit, this isn’t at all the case. In fact, insulin resistance is only a symptom of the problem.

Why Would Sugar Cause Insulin Resistance and Diabetes?

Carbohydrates, specifically sugar, are typically blamed for insulin resistance and diabetes for 2 reasons:

1. Carbohydrates increase blood sugar, which increases the secretion of insulin. It’s assumed that as our bodies secrete and use more insulin, our cells become less sensitive to it.

This idea clearly reflects the mechanical, reductionist view of the human body that permeates conventional medicine. This view focuses heavily on symptoms, and therefore has a tendency to blame the symptoms for causing the disease or condition.

In the case of insulin resistance and diabetes, this has taken the form of blaming foods that raise blood sugar and increase insulin secretion. (The same has happened with heart disease and cholesterol, as I explained here)

But, just because blood sugar increases and insulin can’t properly function in these conditions doesn’t mean that insulin resistance and diabetes are caused by too much insulin or the raising of blood sugar.

Aside from this idea being born out of the mechanical and reductionistic views of the human body, there is little evidence, if any, supporting that cells become less sensitive to insulin as they’re exposed to more insulin or higher blood sugar levels.

However, there is substantial evidence against this idea, including that high carbohydrate and sugar intakes are not associated with insulin resistance and diabetes (3, 4, 5, 6, 7). And, that increasing carbohydrate consumption actually increases insulin sensitivity (the opposite of insulin resistance) (8, 9, 10, 11, 12).

When considering that our bodies complex, adaptive systems, this isn’t surprising. Instead, it’s the expected, logical adaption to increased carbohydrate intake.

2. Carbohydrates, specifically fructose, can stimulate inflammatory pathways that cause insulin resistance.

Fructose doesn’t raise the blood sugar and increase insulin like most carbohydrates, but it’s considered the culprit for insulin resistance due to its “inflammatory and fat-producing effects.”

However, as I explained here and here, sugar, and specifically fructose, doesn’t cause inflammation and fat-production in humans unless it’s consumed in extremely large quantities (like the equivalent of 40 cans of soda over 2 days) or it isn’t being efficiently used to produce energy (we’ll talk more about this in a little bit). And, the inflammation it causes is very different from the chronic inflammation that underlies chronic diseases.

One thing that I didn’t mention in those articles is that when those inflammatory and fat-producing pathways are stimulated, they also cause insulin resistance.

But, like the “inflammation,” this insulin resistance is only temporary and doesn’t have the same consequences as the insulin resistance in metabolic syndrome and diabetes.

Instead, this temporary insulin resistance is a protective mechanism that stops more fructose from entering a liver that already has more than enough fructose. But as the liver uses this fructose, the insulin resistance dissipates.

This temporary insulin resistance is similar to the insulin resistance seen in response to low-carb and ketogenic diets, which often dissipates once the body becomes accustomed to glucose metabolism, as talked about here.

It may sound like I’m saying that not all insulin resistance is the same. And, that’s kind of true, but it would be more accurate to say that insulin resistance is only one part of the picture. The important question is why is the insulin resistance there?

It All Comes Down to Energy

As I mentioned earlier, the conventional idea that insulin resistance occurs because our cells no longer respond as well to insulin, preventing them from getting enough sugar, is a fallacy. In fact, insulin resistance isn’t the problem at all, but we’ll get to that in a second.

The problem in diabetes isn’t that the cells can’t get enough sugar, it’s that they can’t use the sugar they have to produce energy (13, 14, 15, 16). Because sugar isn’t being used to produce energy, it builds up in the cells. This blocks more sugar from entering the cells, which prevents insulin from doing its job (15).

In this situation, even giving someone extra insulin doesn’t increase the amount of sugar that enters the cells or the amount of sugar used to produce energy (13, 14, 17).

Plus, because sugar can’t enter the cells it remains in the blood, which partially accounts for the high blood sugar seen in diabetes.

And, due to the cells’ inability to use sugar to produce energy, those with diabetes have elevated levels of glucagon and cortisol, which are typically elevated under conditions of low blood sugar (or more accurately, low energy supply), despite the high blood sugar seen in diabetes (18, 19, 20).

These stress hormones cause the liver to continue to release large amounts of sugar, which is largely responsible for the high blood sugar seen in diabetes (17).

In other words, insulin resistance isn’t really the problem in diabetes! The problem is an inability to use sugar to produce energy, which inhibits the function of insulin. The lack of energy also causes high levels of glucagon and cortisol, which cause the liver to release large amounts of sugar and results in high blood sugar.

Instead of being the underlying problem, insulin resistance is simply the way that our cells say “we don’t need any more fuel.”

It can happen under conditions of extreme fructose excess or a low-carb/ketogenic diet, as was mentioned earlier. But, it’s really only a symptom of a problem when energy production is inhibited (like in diabetes), in which case the real problem is the lack of energy!

With that in mind, carbohydrates, including sugar, are most definitely not the cause of insulin resistance and diabetes. And, avoiding carbohydrates simply avoids the problem rather than solving it.

If you want to learn more about what actually causes type 2 diabetes and insulin resistance, check out this video. And, make sure to sign up for the free mini-course below, where you’ll learn how you can correct energy production and usage in order to improve these conditions!

References

Sugar Does NOT Cause Insulin Resistance or Diabetes

Insulin resistance is one of the main components of metabolic syndrome, which increases heart disease risk, diabetes risk, and overall mortality (1).

Diabetes and prediabetes, which are considered to be a result of insulin resistance, have reached epidemic levels. 114 million U.S. adults have diabetes or prediabetes, accounting for a staggering 35% of the entire U.S. population! (2) And the numbers are only increasing.

The worst part is that the current recommendations for handling insulin resistance and diabetes only make them worse. These recommendations center around the mistaken belief that the consumption of carbohydrates, specifically sugar, is to blame for causing and worsening these conditions.

This is a huge problem, to say the least.

What are Insulin Resistance and Diabetes?

Insulin is one of the regulators of our blood sugar.

When we consume any form of carbohydrates, including sugars, our blood sugar increases. The increase in blood sugar triggers the release of insulin, which allows sugar to move from the blood into the cells where it can be used to produce energy.

The conventional view of insulin resistance is that the cells don’t respond as well to insulin (they “resist” insulin’s effects), so the sugar isn’t moved from the blood into the cells, causing blood sugar levels to remain slightly elevated. Diabetes (type 2) is considered to be the result of a more intense form of insulin resistance, where the cells respond even less to insulin and blood sugar levels remain very high.

From this view, the problem in insulin resistance and diabetes is that sugar can’t be transported into the cells where it’s needed. But, as you’ll read in a little bit, this isn’t at all the case. In fact, insulin resistance is only a symptom of the problem.

Why Would Sugar Cause Insulin Resistance and Diabetes?

Carbohydrates, specifically sugar, are typically blamed for insulin resistance and diabetes for 2 reasons:

1. Carbohydrates increase blood sugar, which increases the secretion of insulin. It’s assumed that as our bodies secrete and use more insulin, our cells become less sensitive to it.

This idea clearly reflects the mechanical, reductionist view of the human body that permeates conventional medicine. This view focuses heavily on symptoms, and therefore has a tendency to blame the symptoms for causing the disease or condition.

In the case of insulin resistance and diabetes, this has taken the form of blaming foods that raise blood sugar and increase insulin secretion. (The same has happened with heart disease and cholesterol, as I explained here)

But, just because blood sugar increases and insulin can’t properly function in these conditions doesn’t mean that insulin resistance and diabetes are caused by too much insulin or the raising of blood sugar.

Aside from this idea being born out of the mechanical and reductionistic views of the human body, there is little evidence, if any, supporting that cells become less sensitive to insulin as they’re exposed to more insulin or higher blood sugar levels.

However, there is substantial evidence against this idea, including that high carbohydrate and sugar intakes are not associated with insulin resistance and diabetes (3, 4, 5, 6, 7). And, that increasing carbohydrate consumption actually increases insulin sensitivity (the opposite of insulin resistance) (8, 9, 10, 11, 12).

When considering that our bodies complex, adaptive systems, this isn’t surprising. Instead, it’s the expected, logical adaption to increased carbohydrate intake.

2. Carbohydrates, specifically fructose, can stimulate inflammatory pathways that cause insulin resistance.

Fructose doesn’t raise the blood sugar and increase insulin like most carbohydrates, but it’s considered the culprit for insulin resistance due to its “inflammatory and fat-producing effects.”

However, as I explained here and here, sugar, and specifically fructose, doesn’t cause inflammation and fat-production in humans unless it’s consumed in extremely large quantities (like the equivalent of 40 cans of soda over 2 days) or it isn’t being efficiently used to produce energy (we’ll talk more about this in a little bit). And, the inflammation it causes is very different from the chronic inflammation that underlies chronic diseases.

One thing that I didn’t mention in those articles is that when those inflammatory and fat-producing pathways are stimulated, they also cause insulin resistance.

But, like the “inflammation,” this insulin resistance is only temporary and doesn’t have the same consequences as the insulin resistance in metabolic syndrome and diabetes.

Instead, this temporary insulin resistance is a protective mechanism that stops more fructose from entering a liver that already has more than enough fructose. But as the liver uses this fructose, the insulin resistance dissipates.

This temporary insulin resistance is similar to the insulin resistance seen in response to low-carb and ketogenic diets, which often dissipates once the body becomes accustomed to glucose metabolism, as talked about here.

It may sound like I’m saying that not all insulin resistance is the same. And, that’s kind of true, but it would be more accurate to say that insulin resistance is only one part of the picture. The important question is why is the insulin resistance there?

It All Comes Down to Energy

As I mentioned earlier, the conventional idea that insulin resistance occurs because our cells no longer respond as well to insulin, preventing them from getting enough sugar, is a fallacy. In fact, insulin resistance isn’t the problem at all, but we’ll get to that in a second.

The problem in diabetes isn’t that the cells can’t get enough sugar, it’s that they can’t use the sugar they have to produce energy (13, 14, 15, 16). Because sugar isn’t being used to produce energy, it builds up in the cells. This blocks more sugar from entering the cells, which prevents insulin from doing its job (15).

In this situation, even giving someone extra insulin doesn’t increase the amount of sugar that enters the cells or the amount of sugar used to produce energy (13, 14, 17).

Plus, because sugar can’t enter the cells it remains in the blood, which partially accounts for the high blood sugar seen in diabetes.

And, due to the cells’ inability to use sugar to produce energy, those with diabetes have elevated levels of glucagon and cortisol, which are typically elevated under conditions of low blood sugar (or more accurately, low energy supply), despite the high blood sugar seen in diabetes (18, 19, 20).

These stress hormones cause the liver to continue to release large amounts of sugar, which is largely responsible for the high blood sugar seen in diabetes (17).

In other words, insulin resistance isn’t really the problem in diabetes! The problem is an inability to use sugar to produce energy, which inhibits the function of insulin. The lack of energy also causes high levels of glucagon and cortisol, which cause the liver to release large amounts of sugar and results in high blood sugar.

Instead of being the underlying problem, insulin resistance is simply the way that our cells say “we don’t need any more fuel.”

It can happen under conditions of extreme fructose excess or a low-carb/ketogenic diet, as was mentioned earlier. But, it’s really only a symptom of a problem when energy production is inhibited (like in diabetes), in which case the real problem is the lack of energy!

With that in mind, carbohydrates, including sugar, are most definitely not the cause of insulin resistance and diabetes. And, avoiding carbohydrates simply avoids the problem rather than solving it.

If you want to learn more about what actually causes type 2 diabetes and insulin resistance, check out this video. And, make sure to sign up for the free mini-course below, where you’ll learn how you can correct energy production and usage in order to improve these conditions!

References

Sugar Does NOT Cause Insulin Resistance or Diabetes

Insulin resistance is one of the main components of metabolic syndrome, which increases heart disease risk, diabetes risk, and overall mortality (1).

Diabetes and prediabetes, which are considered to be a result of insulin resistance, have reached epidemic levels. 114 million U.S. adults have diabetes or prediabetes, accounting for a staggering 35% of the entire U.S. population! (2) And the numbers are only increasing.

The worst part is that the current recommendations for handling insulin resistance and diabetes only make them worse. These recommendations center around the mistaken belief that the consumption of carbohydrates, specifically sugar, is to blame for causing and worsening these conditions.

This is a huge problem, to say the least.

What are Insulin Resistance and Diabetes?

Insulin is one of the regulators of our blood sugar.

When we consume any form of carbohydrates, including sugars, our blood sugar increases. The increase in blood sugar triggers the release of insulin, which allows sugar to move from the blood into the cells where it can be used to produce energy.

The conventional view of insulin resistance is that the cells don’t respond as well to insulin (they “resist” insulin’s effects), so the sugar isn’t moved from the blood into the cells, causing blood sugar levels to remain slightly elevated. Diabetes (type 2) is considered to be the result of a more intense form of insulin resistance, where the cells respond even less to insulin and blood sugar levels remain very high.

From this view, the problem in insulin resistance and diabetes is that sugar can’t be transported into the cells where it’s needed. But, as you’ll read in a little bit, this isn’t at all the case. In fact, insulin resistance is only a symptom of the problem.

Why Would Sugar Cause Insulin Resistance and Diabetes?

Carbohydrates, specifically sugar, are typically blamed for insulin resistance and diabetes for 2 reasons:

1. Carbohydrates increase blood sugar, which increases the secretion of insulin. It’s assumed that as our bodies secrete and use more insulin, our cells become less sensitive to it.

This idea clearly reflects the mechanical, reductionist view of the human body that permeates conventional medicine. This view focuses heavily on symptoms, and therefore has a tendency to blame the symptoms for causing the disease or condition.

In the case of insulin resistance and diabetes, this has taken the form of blaming foods that raise blood sugar and increase insulin secretion. (The same has happened with heart disease and cholesterol, as I explained here)

But, just because blood sugar increases and insulin can’t properly function in these conditions doesn’t mean that insulin resistance and diabetes are caused by too much insulin or the raising of blood sugar.

Aside from this idea being born out of the mechanical and reductionistic views of the human body, there is little evidence, if any, supporting that cells become less sensitive to insulin as they’re exposed to more insulin or higher blood sugar levels.

However, there is substantial evidence against this idea, including that high carbohydrate and sugar intakes are not associated with insulin resistance and diabetes (3, 4, 5, 6, 7). And, that increasing carbohydrate consumption actually increases insulin sensitivity (the opposite of insulin resistance) (8, 9, 10, 11, 12).

When considering that our bodies complex, adaptive systems, this isn’t surprising. Instead, it’s the expected, logical adaption to increased carbohydrate intake.

2. Carbohydrates, specifically fructose, can stimulate inflammatory pathways that cause insulin resistance.

Fructose doesn’t raise the blood sugar and increase insulin like most carbohydrates, but it’s considered the culprit for insulin resistance due to its “inflammatory and fat-producing effects.”

However, as I explained here and here, sugar, and specifically fructose, doesn’t cause inflammation and fat-production in humans unless it’s consumed in extremely large quantities (like the equivalent of 40 cans of soda over 2 days) or it isn’t being efficiently used to produce energy (we’ll talk more about this in a little bit). And, the inflammation it causes is very different from the chronic inflammation that underlies chronic diseases.

One thing that I didn’t mention in those articles is that when those inflammatory and fat-producing pathways are stimulated, they also cause insulin resistance.

But, like the “inflammation,” this insulin resistance is only temporary and doesn’t have the same consequences as the insulin resistance in metabolic syndrome and diabetes.

Instead, this temporary insulin resistance is a protective mechanism that stops more fructose from entering a liver that already has more than enough fructose. But as the liver uses this fructose, the insulin resistance dissipates.

This temporary insulin resistance is similar to the insulin resistance seen in response to low-carb and ketogenic diets, which often dissipates once the body becomes accustomed to glucose metabolism, as talked about here.

It may sound like I’m saying that not all insulin resistance is the same. And, that’s kind of true, but it would be more accurate to say that insulin resistance is only one part of the picture. The important question is why is the insulin resistance there?

It All Comes Down to Energy

As I mentioned earlier, the conventional idea that insulin resistance occurs because our cells no longer respond as well to insulin, preventing them from getting enough sugar, is a fallacy. In fact, insulin resistance isn’t the problem at all, but we’ll get to that in a second.

The problem in diabetes isn’t that the cells can’t get enough sugar, it’s that they can’t use the sugar they have to produce energy (13, 14, 15, 16). Because sugar isn’t being used to produce energy, it builds up in the cells. This blocks more sugar from entering the cells, which prevents insulin from doing its job (15).

In this situation, even giving someone extra insulin doesn’t increase the amount of sugar that enters the cells or the amount of sugar used to produce energy (13, 14, 17).

Plus, because sugar can’t enter the cells it remains in the blood, which partially accounts for the high blood sugar seen in diabetes.

And, due to the cells’ inability to use sugar to produce energy, those with diabetes have elevated levels of glucagon and cortisol, which are typically elevated under conditions of low blood sugar (or more accurately, low energy supply), despite the high blood sugar seen in diabetes (18, 19, 20).

These stress hormones cause the liver to continue to release large amounts of sugar, which is largely responsible for the high blood sugar seen in diabetes (17).

In other words, insulin resistance isn’t really the problem in diabetes! The problem is an inability to use sugar to produce energy, which inhibits the function of insulin. The lack of energy also causes high levels of glucagon and cortisol, which cause the liver to release large amounts of sugar and results in high blood sugar.

Instead of being the underlying problem, insulin resistance is simply the way that our cells say “we don’t need any more fuel.”

It can happen under conditions of extreme fructose excess or a low-carb/ketogenic diet, as was mentioned earlier. But, it’s really only a symptom of a problem when energy production is inhibited (like in diabetes), in which case the real problem is the lack of energy!

With that in mind, carbohydrates, including sugar, are most definitely not the cause of insulin resistance and diabetes. And, avoiding carbohydrates simply avoids the problem rather than solving it.

If you want to learn more about what actually causes type 2 diabetes and insulin resistance, check out this video. And, make sure to sign up for the free mini-course below, where you’ll learn how you can correct energy production and usage in order to improve these conditions!

References

Sugar Does NOT Cause Insulin Resistance or Diabetes

Insulin resistance is one of the main components of metabolic syndrome, which increases heart disease risk, diabetes risk, and overall mortality (1).

Diabetes and prediabetes, which are considered to be a result of insulin resistance, have reached epidemic levels. 114 million U.S. adults have diabetes or prediabetes, accounting for a staggering 35% of the entire U.S. population! (2) And the numbers are only increasing.

The worst part is that the current recommendations for handling insulin resistance and diabetes only make them worse. These recommendations center around the mistaken belief that the consumption of carbohydrates, specifically sugar, is to blame for causing and worsening these conditions.

This is a huge problem, to say the least.

What are Insulin Resistance and Diabetes?

Insulin is one of the regulators of our blood sugar.

When we consume any form of carbohydrates, including sugars, our blood sugar increases. The increase in blood sugar triggers the release of insulin, which allows sugar to move from the blood into the cells where it can be used to produce energy.

The conventional view of insulin resistance is that the cells don’t respond as well to insulin (they “resist” insulin’s effects), so the sugar isn’t moved from the blood into the cells, causing blood sugar levels to remain slightly elevated. Diabetes (type 2) is considered to be the result of a more intense form of insulin resistance, where the cells respond even less to insulin and blood sugar levels remain very high.

From this view, the problem in insulin resistance and diabetes is that sugar can’t be transported into the cells where it’s needed. But, as you’ll read in a little bit, this isn’t at all the case. In fact, insulin resistance is only a symptom of the problem.

Why Would Sugar Cause Insulin Resistance and Diabetes?

Carbohydrates, specifically sugar, are typically blamed for insulin resistance and diabetes for 2 reasons:

1. Carbohydrates increase blood sugar, which increases the secretion of insulin. It’s assumed that as our bodies secrete and use more insulin, our cells become less sensitive to it.

This idea clearly reflects the mechanical, reductionist view of the human body that permeates conventional medicine. This view focuses heavily on symptoms, and therefore has a tendency to blame the symptoms for causing the disease or condition.

In the case of insulin resistance and diabetes, this has taken the form of blaming foods that raise blood sugar and increase insulin secretion. (The same has happened with heart disease and cholesterol, as I explained here)

But, just because blood sugar increases and insulin can’t properly function in these conditions doesn’t mean that insulin resistance and diabetes are caused by too much insulin or the raising of blood sugar.

Aside from this idea being born out of the mechanical and reductionistic views of the human body, there is little evidence, if any, supporting that cells become less sensitive to insulin as they’re exposed to more insulin or higher blood sugar levels.

However, there is substantial evidence against this idea, including that high carbohydrate and sugar intakes are not associated with insulin resistance and diabetes (3, 4, 5, 6, 7). And, that increasing carbohydrate consumption actually increases insulin sensitivity (the opposite of insulin resistance) (8, 9, 10, 11, 12).

When considering that our bodies complex, adaptive systems, this isn’t surprising. Instead, it’s the expected, logical adaption to increased carbohydrate intake.

2. Carbohydrates, specifically fructose, can stimulate inflammatory pathways that cause insulin resistance.

Fructose doesn’t raise the blood sugar and increase insulin like most carbohydrates, but it’s considered the culprit for insulin resistance due to its “inflammatory and fat-producing effects.”

However, as I explained here and here, sugar, and specifically fructose, doesn’t cause inflammation and fat-production in humans unless it’s consumed in extremely large quantities (like the equivalent of 40 cans of soda over 2 days) or it isn’t being efficiently used to produce energy (we’ll talk more about this in a little bit). And, the inflammation it causes is very different from the chronic inflammation that underlies chronic diseases.

One thing that I didn’t mention in those articles is that when those inflammatory and fat-producing pathways are stimulated, they also cause insulin resistance.

But, like the “inflammation,” this insulin resistance is only temporary and doesn’t have the same consequences as the insulin resistance in metabolic syndrome and diabetes.

Instead, this temporary insulin resistance is a protective mechanism that stops more fructose from entering a liver that already has more than enough fructose. But as the liver uses this fructose, the insulin resistance dissipates.

This temporary insulin resistance is similar to the insulin resistance seen in response to low-carb and ketogenic diets, which often dissipates once the body becomes accustomed to glucose metabolism, as talked about here.

It may sound like I’m saying that not all insulin resistance is the same. And, that’s kind of true, but it would be more accurate to say that insulin resistance is only one part of the picture. The important question is why is the insulin resistance there?

It All Comes Down to Energy

As I mentioned earlier, the conventional idea that insulin resistance occurs because our cells no longer respond as well to insulin, preventing them from getting enough sugar, is a fallacy. In fact, insulin resistance isn’t the problem at all, but we’ll get to that in a second.

The problem in diabetes isn’t that the cells can’t get enough sugar, it’s that they can’t use the sugar they have to produce energy (13, 14, 15, 16). Because sugar isn’t being used to produce energy, it builds up in the cells. This blocks more sugar from entering the cells, which prevents insulin from doing its job (15).

In this situation, even giving someone extra insulin doesn’t increase the amount of sugar that enters the cells or the amount of sugar used to produce energy (13, 14, 17).

Plus, because sugar can’t enter the cells it remains in the blood, which partially accounts for the high blood sugar seen in diabetes.

And, due to the cells’ inability to use sugar to produce energy, those with diabetes have elevated levels of glucagon and cortisol, which are typically elevated under conditions of low blood sugar (or more accurately, low energy supply), despite the high blood sugar seen in diabetes (18, 19, 20).

These stress hormones cause the liver to continue to release large amounts of sugar, which is largely responsible for the high blood sugar seen in diabetes (17).

In other words, insulin resistance isn’t really the problem in diabetes! The problem is an inability to use sugar to produce energy, which inhibits the function of insulin. The lack of energy also causes high levels of glucagon and cortisol, which cause the liver to release large amounts of sugar and results in high blood sugar.

Instead of being the underlying problem, insulin resistance is simply the way that our cells say “we don’t need any more fuel.”

It can happen under conditions of extreme fructose excess or a low-carb/ketogenic diet, as was mentioned earlier. But, it’s really only a symptom of a problem when energy production is inhibited (like in diabetes), in which case the real problem is the lack of energy!

With that in mind, carbohydrates, including sugar, are most definitely not the cause of insulin resistance and diabetes. And, avoiding carbohydrates simply avoids the problem rather than solving it.

If you want to learn more about what actually causes type 2 diabetes and insulin resistance, check out this video. And, make sure to sign up for the free mini-course below, where you’ll learn how you can correct energy production and usage in order to improve these conditions!

References

Sugar Does NOT Cause Insulin Resistance or Diabetes

Insulin resistance is one of the main components of metabolic syndrome, which increases heart disease risk, diabetes risk, and overall mortality (1).

Diabetes and prediabetes, which are considered to be a result of insulin resistance, have reached epidemic levels. 114 million U.S. adults have diabetes or prediabetes, accounting for a staggering 35% of the entire U.S. population! (2) And the numbers are only increasing.

The worst part is that the current recommendations for handling insulin resistance and diabetes only make them worse. These recommendations center around the mistaken belief that the consumption of carbohydrates, specifically sugar, is to blame for causing and worsening these conditions.

This is a huge problem, to say the least.

What are Insulin Resistance and Diabetes?

Insulin is one of the regulators of our blood sugar.

When we consume any form of carbohydrates, including sugars, our blood sugar increases. The increase in blood sugar triggers the release of insulin, which allows sugar to move from the blood into the cells where it can be used to produce energy.

The conventional view of insulin resistance is that the cells don’t respond as well to insulin (they “resist” insulin’s effects), so the sugar isn’t moved from the blood into the cells, causing blood sugar levels to remain slightly elevated. Diabetes (type 2) is considered to be the result of a more intense form of insulin resistance, where the cells respond even less to insulin and blood sugar levels remain very high.

From this view, the problem in insulin resistance and diabetes is that sugar can’t be transported into the cells where it’s needed. But, as you’ll read in a little bit, this isn’t at all the case. In fact, insulin resistance is only a symptom of the problem.

Why Would Sugar Cause Insulin Resistance and Diabetes?

Carbohydrates, specifically sugar, are typically blamed for insulin resistance and diabetes for 2 reasons:

1. Carbohydrates increase blood sugar, which increases the secretion of insulin. It’s assumed that as our bodies secrete and use more insulin, our cells become less sensitive to it.

This idea clearly reflects the mechanical, reductionist view of the human body that permeates conventional medicine. This view focuses heavily on symptoms, and therefore has a tendency to blame the symptoms for causing the disease or condition.

In the case of insulin resistance and diabetes, this has taken the form of blaming foods that raise blood sugar and increase insulin secretion. (The same has happened with heart disease and cholesterol, as I explained here)

But, just because blood sugar increases and insulin can’t properly function in these conditions doesn’t mean that insulin resistance and diabetes are caused by too much insulin or the raising of blood sugar.

Aside from this idea being born out of the mechanical and reductionistic views of the human body, there is little evidence, if any, supporting that cells become less sensitive to insulin as they’re exposed to more insulin or higher blood sugar levels.

However, there is substantial evidence against this idea, including that high carbohydrate and sugar intakes are not associated with insulin resistance and diabetes (3, 4, 5, 6, 7). And, that increasing carbohydrate consumption actually increases insulin sensitivity (the opposite of insulin resistance) (8, 9, 10, 11, 12).

When considering that our bodies complex, adaptive systems, this isn’t surprising. Instead, it’s the expected, logical adaption to increased carbohydrate intake.

2. Carbohydrates, specifically fructose, can stimulate inflammatory pathways that cause insulin resistance.

Fructose doesn’t raise the blood sugar and increase insulin like most carbohydrates, but it’s considered the culprit for insulin resistance due to its “inflammatory and fat-producing effects.”

However, as I explained here and here, sugar, and specifically fructose, doesn’t cause inflammation and fat-production in humans unless it’s consumed in extremely large quantities (like the equivalent of 40 cans of soda over 2 days) or it isn’t being efficiently used to produce energy (we’ll talk more about this in a little bit). And, the inflammation it causes is very different from the chronic inflammation that underlies chronic diseases.

One thing that I didn’t mention in those articles is that when those inflammatory and fat-producing pathways are stimulated, they also cause insulin resistance.

But, like the “inflammation,” this insulin resistance is only temporary and doesn’t have the same consequences as the insulin resistance in metabolic syndrome and diabetes.

Instead, this temporary insulin resistance is a protective mechanism that stops more fructose from entering a liver that already has more than enough fructose. But as the liver uses this fructose, the insulin resistance dissipates.

This temporary insulin resistance is similar to the insulin resistance seen in response to low-carb and ketogenic diets, which often dissipates once the body becomes accustomed to glucose metabolism, as talked about here.

It may sound like I’m saying that not all insulin resistance is the same. And, that’s kind of true, but it would be more accurate to say that insulin resistance is only one part of the picture. The important question is why is the insulin resistance there?

It All Comes Down to Energy

As I mentioned earlier, the conventional idea that insulin resistance occurs because our cells no longer respond as well to insulin, preventing them from getting enough sugar, is a fallacy. In fact, insulin resistance isn’t the problem at all, but we’ll get to that in a second.

The problem in diabetes isn’t that the cells can’t get enough sugar, it’s that they can’t use the sugar they have to produce energy (13, 14, 15, 16). Because sugar isn’t being used to produce energy, it builds up in the cells. This blocks more sugar from entering the cells, which prevents insulin from doing its job (15).

In this situation, even giving someone extra insulin doesn’t increase the amount of sugar that enters the cells or the amount of sugar used to produce energy (13, 14, 17).

Plus, because sugar can’t enter the cells it remains in the blood, which partially accounts for the high blood sugar seen in diabetes.

And, due to the cells’ inability to use sugar to produce energy, those with diabetes have elevated levels of glucagon and cortisol, which are typically elevated under conditions of low blood sugar (or more accurately, low energy supply), despite the high blood sugar seen in diabetes (18, 19, 20).

These stress hormones cause the liver to continue to release large amounts of sugar, which is largely responsible for the high blood sugar seen in diabetes (17).

In other words, insulin resistance isn’t really the problem in diabetes! The problem is an inability to use sugar to produce energy, which inhibits the function of insulin. The lack of energy also causes high levels of glucagon and cortisol, which cause the liver to release large amounts of sugar and results in high blood sugar.

Instead of being the underlying problem, insulin resistance is simply the way that our cells say “we don’t need any more fuel.”

It can happen under conditions of extreme fructose excess or a low-carb/ketogenic diet, as was mentioned earlier. But, it’s really only a symptom of a problem when energy production is inhibited (like in diabetes), in which case the real problem is the lack of energy!

With that in mind, carbohydrates, including sugar, are most definitely not the cause of insulin resistance and diabetes. And, avoiding carbohydrates simply avoids the problem rather than solving it.

If you want to learn more about what actually causes type 2 diabetes and insulin resistance, check out this video. And, make sure to sign up for the free mini-course below, where you’ll learn how you can correct energy production and usage in order to improve these conditions!

References

Sugar Does NOT Cause Insulin Resistance or Diabetes

Insulin resistance is one of the main components of metabolic syndrome, which increases heart disease risk, diabetes risk, and overall mortality (1).

Diabetes and prediabetes, which are considered to be a result of insulin resistance, have reached epidemic levels. 114 million U.S. adults have diabetes or prediabetes, accounting for a staggering 35% of the entire U.S. population! (2) And the numbers are only increasing.

The worst part is that the current recommendations for handling insulin resistance and diabetes only make them worse. These recommendations center around the mistaken belief that the consumption of carbohydrates, specifically sugar, is to blame for causing and worsening these conditions.

This is a huge problem, to say the least.

What are Insulin Resistance and Diabetes?

Insulin is one of the regulators of our blood sugar.

When we consume any form of carbohydrates, including sugars, our blood sugar increases. The increase in blood sugar triggers the release of insulin, which allows sugar to move from the blood into the cells where it can be used to produce energy.

The conventional view of insulin resistance is that the cells don’t respond as well to insulin (they “resist” insulin’s effects), so the sugar isn’t moved from the blood into the cells, causing blood sugar levels to remain slightly elevated. Diabetes (type 2) is considered to be the result of a more intense form of insulin resistance, where the cells respond even less to insulin and blood sugar levels remain very high.

From this view, the problem in insulin resistance and diabetes is that sugar can’t be transported into the cells where it’s needed. But, as you’ll read in a little bit, this isn’t at all the case. In fact, insulin resistance is only a symptom of the problem.

Why Would Sugar Cause Insulin Resistance and Diabetes?

Carbohydrates, specifically sugar, are typically blamed for insulin resistance and diabetes for 2 reasons:

1. Carbohydrates increase blood sugar, which increases the secretion of insulin. It’s assumed that as our bodies secrete and use more insulin, our cells become less sensitive to it.

This idea clearly reflects the mechanical, reductionist view of the human body that permeates conventional medicine. This view focuses heavily on symptoms, and therefore has a tendency to blame the symptoms for causing the disease or condition.

In the case of insulin resistance and diabetes, this has taken the form of blaming foods that raise blood sugar and increase insulin secretion. (The same has happened with heart disease and cholesterol, as I explained here)

But, just because blood sugar increases and insulin can’t properly function in these conditions doesn’t mean that insulin resistance and diabetes are caused by too much insulin or the raising of blood sugar.

Aside from this idea being born out of the mechanical and reductionistic views of the human body, there is little evidence, if any, supporting that cells become less sensitive to insulin as they’re exposed to more insulin or higher blood sugar levels.

However, there is substantial evidence against this idea, including that high carbohydrate and sugar intakes are not associated with insulin resistance and diabetes (3, 4, 5, 6, 7). And, that increasing carbohydrate consumption actually increases insulin sensitivity (the opposite of insulin resistance) (8, 9, 10, 11, 12).

When considering that our bodies complex, adaptive systems, this isn’t surprising. Instead, it’s the expected, logical adaption to increased carbohydrate intake.

2. Carbohydrates, specifically fructose, can stimulate inflammatory pathways that cause insulin resistance.

Fructose doesn’t raise the blood sugar and increase insulin like most carbohydrates, but it’s considered the culprit for insulin resistance due to its “inflammatory and fat-producing effects.”

However, as I explained here and here, sugar, and specifically fructose, doesn’t cause inflammation and fat-production in humans unless it’s consumed in extremely large quantities (like the equivalent of 40 cans of soda over 2 days) or it isn’t being efficiently used to produce energy (we’ll talk more about this in a little bit). And, the inflammation it causes is very different from the chronic inflammation that underlies chronic diseases.

One thing that I didn’t mention in those articles is that when those inflammatory and fat-producing pathways are stimulated, they also cause insulin resistance.

But, like the “inflammation,” this insulin resistance is only temporary and doesn’t have the same consequences as the insulin resistance in metabolic syndrome and diabetes.

Instead, this temporary insulin resistance is a protective mechanism that stops more fructose from entering a liver that already has more than enough fructose. But as the liver uses this fructose, the insulin resistance dissipates.

This temporary insulin resistance is similar to the insulin resistance seen in response to low-carb and ketogenic diets, which often dissipates once the body becomes accustomed to glucose metabolism, as talked about here.

It may sound like I’m saying that not all insulin resistance is the same. And, that’s kind of true, but it would be more accurate to say that insulin resistance is only one part of the picture. The important question is why is the insulin resistance there?

It All Comes Down to Energy

As I mentioned earlier, the conventional idea that insulin resistance occurs because our cells no longer respond as well to insulin, preventing them from getting enough sugar, is a fallacy. In fact, insulin resistance isn’t the problem at all, but we’ll get to that in a second.

The problem in diabetes isn’t that the cells can’t get enough sugar, it’s that they can’t use the sugar they have to produce energy (13, 14, 15, 16). Because sugar isn’t being used to produce energy, it builds up in the cells. This blocks more sugar from entering the cells, which prevents insulin from doing its job (15).

In this situation, even giving someone extra insulin doesn’t increase the amount of sugar that enters the cells or the amount of sugar used to produce energy (13, 14, 17).

Plus, because sugar can’t enter the cells it remains in the blood, which partially accounts for the high blood sugar seen in diabetes.

And, due to the cells’ inability to use sugar to produce energy, those with diabetes have elevated levels of glucagon and cortisol, which are typically elevated under conditions of low blood sugar (or more accurately, low energy supply), despite the high blood sugar seen in diabetes (18, 19, 20).

These stress hormones cause the liver to continue to release large amounts of sugar, which is largely responsible for the high blood sugar seen in diabetes (17).

In other words, insulin resistance isn’t really the problem in diabetes! The problem is an inability to use sugar to produce energy, which inhibits the function of insulin. The lack of energy also causes high levels of glucagon and cortisol, which cause the liver to release large amounts of sugar and results in high blood sugar.

Instead of being the underlying problem, insulin resistance is simply the way that our cells say “we don’t need any more fuel.”

It can happen under conditions of extreme fructose excess or a low-carb/ketogenic diet, as was mentioned earlier. But, it’s really only a symptom of a problem when energy production is inhibited (like in diabetes), in which case the real problem is the lack of energy!

With that in mind, carbohydrates, including sugar, are most definitely not the cause of insulin resistance and diabetes. And, avoiding carbohydrates simply avoids the problem rather than solving it.

If you want to learn more about what actually causes type 2 diabetes and insulin resistance, check out this video. And, make sure to sign up for the free mini-course below, where you’ll learn how you can correct energy production and usage in order to improve these conditions!

References

Sugar Does NOT Cause Insulin Resistance or Diabetes

Insulin resistance is one of the main components of metabolic syndrome, which increases heart disease risk, diabetes risk, and overall mortality (1).

Diabetes and prediabetes, which are considered to be a result of insulin resistance, have reached epidemic levels. 114 million U.S. adults have diabetes or prediabetes, accounting for a staggering 35% of the entire U.S. population! (2) And the numbers are only increasing.

The worst part is that the current recommendations for handling insulin resistance and diabetes only make them worse. These recommendations center around the mistaken belief that the consumption of carbohydrates, specifically sugar, is to blame for causing and worsening these conditions.

This is a huge problem, to say the least.

What are Insulin Resistance and Diabetes?

Insulin is one of the regulators of our blood sugar.

When we consume any form of carbohydrates, including sugars, our blood sugar increases. The increase in blood sugar triggers the release of insulin, which allows sugar to move from the blood into the cells where it can be used to produce energy.

The conventional view of insulin resistance is that the cells don’t respond as well to insulin (they “resist” insulin’s effects), so the sugar isn’t moved from the blood into the cells, causing blood sugar levels to remain slightly elevated. Diabetes (type 2) is considered to be the result of a more intense form of insulin resistance, where the cells respond even less to insulin and blood sugar levels remain very high.

From this view, the problem in insulin resistance and diabetes is that sugar can’t be transported into the cells where it’s needed. But, as you’ll read in a little bit, this isn’t at all the case. In fact, insulin resistance is only a symptom of the problem.

Why Would Sugar Cause Insulin Resistance and Diabetes?

Carbohydrates, specifically sugar, are typically blamed for insulin resistance and diabetes for 2 reasons:

1. Carbohydrates increase blood sugar, which increases the secretion of insulin. It’s assumed that as our bodies secrete and use more insulin, our cells become less sensitive to it.

This idea clearly reflects the mechanical, reductionist view of the human body that permeates conventional medicine. This view focuses heavily on symptoms, and therefore has a tendency to blame the symptoms for causing the disease or condition.

In the case of insulin resistance and diabetes, this has taken the form of blaming foods that raise blood sugar and increase insulin secretion. (The same has happened with heart disease and cholesterol, as I explained here)

But, just because blood sugar increases and insulin can’t properly function in these conditions doesn’t mean that insulin resistance and diabetes are caused by too much insulin or the raising of blood sugar.

Aside from this idea being born out of the mechanical and reductionistic views of the human body, there is little evidence, if any, supporting that cells become less sensitive to insulin as they’re exposed to more insulin or higher blood sugar levels.

However, there is substantial evidence against this idea, including that high carbohydrate and sugar intakes are not associated with insulin resistance and diabetes (3, 4, 5, 6, 7). And, that increasing carbohydrate consumption actually increases insulin sensitivity (the opposite of insulin resistance) (8, 9, 10, 11, 12).

When considering that our bodies complex, adaptive systems, this isn’t surprising. Instead, it’s the expected, logical adaption to increased carbohydrate intake.

2. Carbohydrates, specifically fructose, can stimulate inflammatory pathways that cause insulin resistance.

Fructose doesn’t raise the blood sugar and increase insulin like most carbohydrates, but it’s considered the culprit for insulin resistance due to its “inflammatory and fat-producing effects.”

However, as I explained here and here, sugar, and specifically fructose, doesn’t cause inflammation and fat-production in humans unless it’s consumed in extremely large quantities (like the equivalent of 40 cans of soda over 2 days) or it isn’t being efficiently used to produce energy (we’ll talk more about this in a little bit). And, the inflammation it causes is very different from the chronic inflammation that underlies chronic diseases.

One thing that I didn’t mention in those articles is that when those inflammatory and fat-producing pathways are stimulated, they also cause insulin resistance.

But, like the “inflammation,” this insulin resistance is only temporary and doesn’t have the same consequences as the insulin resistance in metabolic syndrome and diabetes.

Instead, this temporary insulin resistance is a protective mechanism that stops more fructose from entering a liver that already has more than enough fructose. But as the liver uses this fructose, the insulin resistance dissipates.

This temporary insulin resistance is similar to the insulin resistance seen in response to low-carb and ketogenic diets, which often dissipates once the body becomes accustomed to glucose metabolism, as talked about here.

It may sound like I’m saying that not all insulin resistance is the same. And, that’s kind of true, but it would be more accurate to say that insulin resistance is only one part of the picture. The important question is why is the insulin resistance there?

It All Comes Down to Energy

As I mentioned earlier, the conventional idea that insulin resistance occurs because our cells no longer respond as well to insulin, preventing them from getting enough sugar, is a fallacy. In fact, insulin resistance isn’t the problem at all, but we’ll get to that in a second.

The problem in diabetes isn’t that the cells can’t get enough sugar, it’s that they can’t use the sugar they have to produce energy (13, 14, 15, 16). Because sugar isn’t being used to produce energy, it builds up in the cells. This blocks more sugar from entering the cells, which prevents insulin from doing its job (15).

In this situation, even giving someone extra insulin doesn’t increase the amount of sugar that enters the cells or the amount of sugar used to produce energy (13, 14, 17).

Plus, because sugar can’t enter the cells it remains in the blood, which partially accounts for the high blood sugar seen in diabetes.

And, due to the cells’ inability to use sugar to produce energy, those with diabetes have elevated levels of glucagon and cortisol, which are typically elevated under conditions of low blood sugar (or more accurately, low energy supply), despite the high blood sugar seen in diabetes (18, 19, 20).

These stress hormones cause the liver to continue to release large amounts of sugar, which is largely responsible for the high blood sugar seen in diabetes (17).

In other words, insulin resistance isn’t really the problem in diabetes! The problem is an inability to use sugar to produce energy, which inhibits the function of insulin. The lack of energy also causes high levels of glucagon and cortisol, which cause the liver to release large amounts of sugar and results in high blood sugar.

Instead of being the underlying problem, insulin resistance is simply the way that our cells say “we don’t need any more fuel.”

It can happen under conditions of extreme fructose excess or a low-carb/ketogenic diet, as was mentioned earlier. But, it’s really only a symptom of a problem when energy production is inhibited (like in diabetes), in which case the real problem is the lack of energy!

With that in mind, carbohydrates, including sugar, are most definitely not the cause of insulin resistance and diabetes. And, avoiding carbohydrates simply avoids the problem rather than solving it.

If you want to learn more about what actually causes type 2 diabetes and insulin resistance, check out this video. And, make sure to sign up for the free mini-course below, where you’ll learn how you can correct energy production and usage in order to improve these conditions!

References

Sugar Does NOT Cause Insulin Resistance or Diabetes

Insulin resistance is one of the main components of metabolic syndrome, which increases heart disease risk, diabetes risk, and overall mortality (1).

Diabetes and prediabetes, which are considered to be a result of insulin resistance, have reached epidemic levels. 114 million U.S. adults have diabetes or prediabetes, accounting for a staggering 35% of the entire U.S. population! (2) And the numbers are only increasing.

The worst part is that the current recommendations for handling insulin resistance and diabetes only make them worse. These recommendations center around the mistaken belief that the consumption of carbohydrates, specifically sugar, is to blame for causing and worsening these conditions.

This is a huge problem, to say the least.

What are Insulin Resistance and Diabetes?

Insulin is one of the regulators of our blood sugar.

When we consume any form of carbohydrates, including sugars, our blood sugar increases. The increase in blood sugar triggers the release of insulin, which allows sugar to move from the blood into the cells where it can be used to produce energy.

The conventional view of insulin resistance is that the cells don’t respond as well to insulin (they “resist” insulin’s effects), so the sugar isn’t moved from the blood into the cells, causing blood sugar levels to remain slightly elevated. Diabetes (type 2) is considered to be the result of a more intense form of insulin resistance, where the cells respond even less to insulin and blood sugar levels remain very high.

From this view, the problem in insulin resistance and diabetes is that sugar can’t be transported into the cells where it’s needed. But, as you’ll read in a little bit, this isn’t at all the case. In fact, insulin resistance is only a symptom of the problem.

Why Would Sugar Cause Insulin Resistance and Diabetes?

Carbohydrates, specifically sugar, are typically blamed for insulin resistance and diabetes for 2 reasons:

1. Carbohydrates increase blood sugar, which increases the secretion of insulin. It’s assumed that as our bodies secrete and use more insulin, our cells become less sensitive to it.

This idea clearly reflects the mechanical, reductionist view of the human body that permeates conventional medicine. This view focuses heavily on symptoms, and therefore has a tendency to blame the symptoms for causing the disease or condition.

In the case of insulin resistance and diabetes, this has taken the form of blaming foods that raise blood sugar and increase insulin secretion. (The same has happened with heart disease and cholesterol, as I explained here)

But, just because blood sugar increases and insulin can’t properly function in these conditions doesn’t mean that insulin resistance and diabetes are caused by too much insulin or the raising of blood sugar.

Aside from this idea being born out of the mechanical and reductionistic views of the human body, there is little evidence, if any, supporting that cells become less sensitive to insulin as they’re exposed to more insulin or higher blood sugar levels.

However, there is substantial evidence against this idea, including that high carbohydrate and sugar intakes are not associated with insulin resistance and diabetes (3, 4, 5, 6, 7). And, that increasing carbohydrate consumption actually increases insulin sensitivity (the opposite of insulin resistance) (8, 9, 10, 11, 12).

When considering that our bodies complex, adaptive systems, this isn’t surprising. Instead, it’s the expected, logical adaption to increased carbohydrate intake.

2. Carbohydrates, specifically fructose, can stimulate inflammatory pathways that cause insulin resistance.

Fructose doesn’t raise the blood sugar and increase insulin like most carbohydrates, but it’s considered the culprit for insulin resistance due to its “inflammatory and fat-producing effects.”

However, as I explained here and here, sugar, and specifically fructose, doesn’t cause inflammation and fat-production in humans unless it’s consumed in extremely large quantities (like the equivalent of 40 cans of soda over 2 days) or it isn’t being efficiently used to produce energy (we’ll talk more about this in a little bit). And, the inflammation it causes is very different from the chronic inflammation that underlies chronic diseases.

One thing that I didn’t mention in those articles is that when those inflammatory and fat-producing pathways are stimulated, they also cause insulin resistance.

But, like the “inflammation,” this insulin resistance is only temporary and doesn’t have the same consequences as the insulin resistance in metabolic syndrome and diabetes.

Instead, this temporary insulin resistance is a protective mechanism that stops more fructose from entering a liver that already has more than enough fructose. But as the liver uses this fructose, the insulin resistance dissipates.

This temporary insulin resistance is similar to the insulin resistance seen in response to low-carb and ketogenic diets, which often dissipates once the body becomes accustomed to glucose metabolism, as talked about here.

It may sound like I’m saying that not all insulin resistance is the same. And, that’s kind of true, but it would be more accurate to say that insulin resistance is only one part of the picture. The important question is why is the insulin resistance there?

It All Comes Down to Energy

As I mentioned earlier, the conventional idea that insulin resistance occurs because our cells no longer respond as well to insulin, preventing them from getting enough sugar, is a fallacy. In fact, insulin resistance isn’t the problem at all, but we’ll get to that in a second.

The problem in diabetes isn’t that the cells can’t get enough sugar, it’s that they can’t use the sugar they have to produce energy (13, 14, 15, 16). Because sugar isn’t being used to produce energy, it builds up in the cells. This blocks more sugar from entering the cells, which prevents insulin from doing its job (15).

In this situation, even giving someone extra insulin doesn’t increase the amount of sugar that enters the cells or the amount of sugar used to produce energy (13, 14, 17).

Plus, because sugar can’t enter the cells it remains in the blood, which partially accounts for the high blood sugar seen in diabetes.

And, due to the cells’ inability to use sugar to produce energy, those with diabetes have elevated levels of glucagon and cortisol, which are typically elevated under conditions of low blood sugar (or more accurately, low energy supply), despite the high blood sugar seen in diabetes (18, 19, 20).

These stress hormones cause the liver to continue to release large amounts of sugar, which is largely responsible for the high blood sugar seen in diabetes (17).

In other words, insulin resistance isn’t really the problem in diabetes! The problem is an inability to use sugar to produce energy, which inhibits the function of insulin. The lack of energy also causes high levels of glucagon and cortisol, which cause the liver to release large amounts of sugar and results in high blood sugar.

Instead of being the underlying problem, insulin resistance is simply the way that our cells say “we don’t need any more fuel.”

It can happen under conditions of extreme fructose excess or a low-carb/ketogenic diet, as was mentioned earlier. But, it’s really only a symptom of a problem when energy production is inhibited (like in diabetes), in which case the real problem is the lack of energy!

With that in mind, carbohydrates, including sugar, are most definitely not the cause of insulin resistance and diabetes. And, avoiding carbohydrates simply avoids the problem rather than solving it.

If you want to learn more about what actually causes type 2 diabetes and insulin resistance, check out this video. And, make sure to sign up for the free mini-course below, where you’ll learn how you can correct energy production and usage in order to improve these conditions!

References

Sugar Does NOT Cause Insulin Resistance or Diabetes

Insulin resistance is one of the main components of metabolic syndrome, which increases heart disease risk, diabetes risk, and overall mortality (1).

Diabetes and prediabetes, which are considered to be a result of insulin resistance, have reached epidemic levels. 114 million U.S. adults have diabetes or prediabetes, accounting for a staggering 35% of the entire U.S. population! (2) And the numbers are only increasing.

The worst part is that the current recommendations for handling insulin resistance and diabetes only make them worse. These recommendations center around the mistaken belief that the consumption of carbohydrates, specifically sugar, is to blame for causing and worsening these conditions.

This is a huge problem, to say the least.

What are Insulin Resistance and Diabetes?

Insulin is one of the regulators of our blood sugar.

When we consume any form of carbohydrates, including sugars, our blood sugar increases. The increase in blood sugar triggers the release of insulin, which allows sugar to move from the blood into the cells where it can be used to produce energy.

The conventional view of insulin resistance is that the cells don’t respond as well to insulin (they “resist” insulin’s effects), so the sugar isn’t moved from the blood into the cells, causing blood sugar levels to remain slightly elevated. Diabetes (type 2) is considered to be the result of a more intense form of insulin resistance, where the cells respond even less to insulin and blood sugar levels remain very high.

From this view, the problem in insulin resistance and diabetes is that sugar can’t be transported into the cells where it’s needed. But, as you’ll read in a little bit, this isn’t at all the case. In fact, insulin resistance is only a symptom of the problem.

Why Would Sugar Cause Insulin Resistance and Diabetes?

Carbohydrates, specifically sugar, are typically blamed for insulin resistance and diabetes for 2 reasons:

1. Carbohydrates increase blood sugar, which increases the secretion of insulin. It’s assumed that as our bodies secrete and use more insulin, our cells become less sensitive to it.

This idea clearly reflects the mechanical, reductionist view of the human body that permeates conventional medicine. This view focuses heavily on symptoms, and therefore has a tendency to blame the symptoms for causing the disease or condition.

In the case of insulin resistance and diabetes, this has taken the form of blaming foods that raise blood sugar and increase insulin secretion. (The same has happened with heart disease and cholesterol, as I explained here)

But, just because blood sugar increases and insulin can’t properly function in these conditions doesn’t mean that insulin resistance and diabetes are caused by too much insulin or the raising of blood sugar.

Aside from this idea being born out of the mechanical and reductionistic views of the human body, there is little evidence, if any, supporting that cells become less sensitive to insulin as they’re exposed to more insulin or higher blood sugar levels.

However, there is substantial evidence against this idea, including that high carbohydrate and sugar intakes are not associated with insulin resistance and diabetes (3, 4, 5, 6, 7). And, that increasing carbohydrate consumption actually increases insulin sensitivity (the opposite of insulin resistance) (8, 9, 10, 11, 12).

When considering that our bodies complex, adaptive systems, this isn’t surprising. Instead, it’s the expected, logical adaption to increased carbohydrate intake.

2. Carbohydrates, specifically fructose, can stimulate inflammatory pathways that cause insulin resistance.

Fructose doesn’t raise the blood sugar and increase insulin like most carbohydrates, but it’s considered the culprit for insulin resistance due to its “inflammatory and fat-producing effects.”

However, as I explained here and here, sugar, and specifically fructose, doesn’t cause inflammation and fat-production in humans unless it’s consumed in extremely large quantities (like the equivalent of 40 cans of soda over 2 days) or it isn’t being efficiently used to produce energy (we’ll talk more about this in a little bit). And, the inflammation it causes is very different from the chronic inflammation that underlies chronic diseases.

One thing that I didn’t mention in those articles is that when those inflammatory and fat-producing pathways are stimulated, they also cause insulin resistance.

But, like the “inflammation,” this insulin resistance is only temporary and doesn’t have the same consequences as the insulin resistance in metabolic syndrome and diabetes.

Instead, this temporary insulin resistance is a protective mechanism that stops more fructose from entering a liver that already has more than enough fructose. But as the liver uses this fructose, the insulin resistance dissipates.

This temporary insulin resistance is similar to the insulin resistance seen in response to low-carb and ketogenic diets, which often dissipates once the body becomes accustomed to glucose metabolism, as talked about here.

It may sound like I’m saying that not all insulin resistance is the same. And, that’s kind of true, but it would be more accurate to say that insulin resistance is only one part of the picture. The important question is why is the insulin resistance there?

It All Comes Down to Energy

As I mentioned earlier, the conventional idea that insulin resistance occurs because our cells no longer respond as well to insulin, preventing them from getting enough sugar, is a fallacy. In fact, insulin resistance isn’t the problem at all, but we’ll get to that in a second.

The problem in diabetes isn’t that the cells can’t get enough sugar, it’s that they can’t use the sugar they have to produce energy (13, 14, 15, 16). Because sugar isn’t being used to produce energy, it builds up in the cells. This blocks more sugar from entering the cells, which prevents insulin from doing its job (15).

In this situation, even giving someone extra insulin doesn’t increase the amount of sugar that enters the cells or the amount of sugar used to produce energy (13, 14, 17).

Plus, because sugar can’t enter the cells it remains in the blood, which partially accounts for the high blood sugar seen in diabetes.

And, due to the cells’ inability to use sugar to produce energy, those with diabetes have elevated levels of glucagon and cortisol, which are typically elevated under conditions of low blood sugar (or more accurately, low energy supply), despite the high blood sugar seen in diabetes (18, 19, 20).

These stress hormones cause the liver to continue to release large amounts of sugar, which is largely responsible for the high blood sugar seen in diabetes (17).

In other words, insulin resistance isn’t really the problem in diabetes! The problem is an inability to use sugar to produce energy, which inhibits the function of insulin. The lack of energy also causes high levels of glucagon and cortisol, which cause the liver to release large amounts of sugar and results in high blood sugar.

Instead of being the underlying problem, insulin resistance is simply the way that our cells say “we don’t need any more fuel.”

It can happen under conditions of extreme fructose excess or a low-carb/ketogenic diet, as was mentioned earlier. But, it’s really only a symptom of a problem when energy production is inhibited (like in diabetes), in which case the real problem is the lack of energy!

With that in mind, carbohydrates, including sugar, are most definitely not the cause of insulin resistance and diabetes. And, avoiding carbohydrates simply avoids the problem rather than solving it.

If you want to learn more about what actually causes type 2 diabetes and insulin resistance, check out this video. And, make sure to sign up for the free mini-course below, where you’ll learn how you can correct energy production and usage in order to improve these conditions!

References

Sugar Does NOT Cause Insulin Resistance or Diabetes

Insulin resistance is one of the main components of metabolic syndrome, which increases heart disease risk, diabetes risk, and overall mortality (1).

Diabetes and prediabetes, which are considered to be a result of insulin resistance, have reached epidemic levels. 114 million U.S. adults have diabetes or prediabetes, accounting for a staggering 35% of the entire U.S. population! (2) And the numbers are only increasing.

The worst part is that the current recommendations for handling insulin resistance and diabetes only make them worse. These recommendations center around the mistaken belief that the consumption of carbohydrates, specifically sugar, is to blame for causing and worsening these conditions.

This is a huge problem, to say the least.

What are Insulin Resistance and Diabetes?

Insulin is one of the regulators of our blood sugar.

When we consume any form of carbohydrates, including sugars, our blood sugar increases. The increase in blood sugar triggers the release of insulin, which allows sugar to move from the blood into the cells where it can be used to produce energy.

The conventional view of insulin resistance is that the cells don’t respond as well to insulin (they “resist” insulin’s effects), so the sugar isn’t moved from the blood into the cells, causing blood sugar levels to remain slightly elevated. Diabetes (type 2) is considered to be the result of a more intense form of insulin resistance, where the cells respond even less to insulin and blood sugar levels remain very high.

From this view, the problem in insulin resistance and diabetes is that sugar can’t be transported into the cells where it’s needed. But, as you’ll read in a little bit, this isn’t at all the case. In fact, insulin resistance is only a symptom of the problem.

Why Would Sugar Cause Insulin Resistance and Diabetes?

Carbohydrates, specifically sugar, are typically blamed for insulin resistance and diabetes for 2 reasons:

1. Carbohydrates increase blood sugar, which increases the secretion of insulin. It’s assumed that as our bodies secrete and use more insulin, our cells become less sensitive to it.

This idea clearly reflects the mechanical, reductionist view of the human body that permeates conventional medicine. This view focuses heavily on symptoms, and therefore has a tendency to blame the symptoms for causing the disease or condition.

In the case of insulin resistance and diabetes, this has taken the form of blaming foods that raise blood sugar and increase insulin secretion. (The same has happened with heart disease and cholesterol, as I explained here)

But, just because blood sugar increases and insulin can’t properly function in these conditions doesn’t mean that insulin resistance and diabetes are caused by too much insulin or the raising of blood sugar.

Aside from this idea being born out of the mechanical and reductionistic views of the human body, there is little evidence, if any, supporting that cells become less sensitive to insulin as they’re exposed to more insulin or higher blood sugar levels.

However, there is substantial evidence against this idea, including that high carbohydrate and sugar intakes are not associated with insulin resistance and diabetes (3, 4, 5, 6, 7). And, that increasing carbohydrate consumption actually increases insulin sensitivity (the opposite of insulin resistance) (8, 9, 10, 11, 12).

When considering that our bodies complex, adaptive systems, this isn’t surprising. Instead, it’s the expected, logical adaption to increased carbohydrate intake.

2. Carbohydrates, specifically fructose, can stimulate inflammatory pathways that cause insulin resistance.

Fructose doesn’t raise the blood sugar and increase insulin like most carbohydrates, but it’s considered the culprit for insulin resistance due to its “inflammatory and fat-producing effects.”

However, as I explained here and here, sugar, and specifically fructose, doesn’t cause inflammation and fat-production in humans unless it’s consumed in extremely large quantities (like the equivalent of 40 cans of soda over 2 days) or it isn’t being efficiently used to produce energy (we’ll talk more about this in a little bit). And, the inflammation it causes is very different from the chronic inflammation that underlies chronic diseases.

One thing that I didn’t mention in those articles is that when those inflammatory and fat-producing pathways are stimulated, they also cause insulin resistance.

But, like the “inflammation,” this insulin resistance is only temporary and doesn’t have the same consequences as the insulin resistance in metabolic syndrome and diabetes.

Instead, this temporary insulin resistance is a protective mechanism that stops more fructose from entering a liver that already has more than enough fructose. But as the liver uses this fructose, the insulin resistance dissipates.

This temporary insulin resistance is similar to the insulin resistance seen in response to low-carb and ketogenic diets, which often dissipates once the body becomes accustomed to glucose metabolism, as talked about here.

It may sound like I’m saying that not all insulin resistance is the same. And, that’s kind of true, but it would be more accurate to say that insulin resistance is only one part of the picture. The important question is why is the insulin resistance there?

It All Comes Down to Energy

As I mentioned earlier, the conventional idea that insulin resistance occurs because our cells no longer respond as well to insulin, preventing them from getting enough sugar, is a fallacy. In fact, insulin resistance isn’t the problem at all, but we’ll get to that in a second.

The problem in diabetes isn’t that the cells can’t get enough sugar, it’s that they can’t use the sugar they have to produce energy (13, 14, 15, 16). Because sugar isn’t being used to produce energy, it builds up in the cells. This blocks more sugar from entering the cells, which prevents insulin from doing its job (15).

In this situation, even giving someone extra insulin doesn’t increase the amount of sugar that enters the cells or the amount of sugar used to produce energy (13, 14, 17).

Plus, because sugar can’t enter the cells it remains in the blood, which partially accounts for the high blood sugar seen in diabetes.

And, due to the cells’ inability to use sugar to produce energy, those with diabetes have elevated levels of glucagon and cortisol, which are typically elevated under conditions of low blood sugar (or more accurately, low energy supply), despite the high blood sugar seen in diabetes (18, 19, 20).

These stress hormones cause the liver to continue to release large amounts of sugar, which is largely responsible for the high blood sugar seen in diabetes (17).

In other words, insulin resistance isn’t really the problem in diabetes! The problem is an inability to use sugar to produce energy, which inhibits the function of insulin. The lack of energy also causes high levels of glucagon and cortisol, which cause the liver to release large amounts of sugar and results in high blood sugar.

Instead of being the underlying problem, insulin resistance is simply the way that our cells say “we don’t need any more fuel.”

It can happen under conditions of extreme fructose excess or a low-carb/ketogenic diet, as was mentioned earlier. But, it’s really only a symptom of a problem when energy production is inhibited (like in diabetes), in which case the real problem is the lack of energy!

With that in mind, carbohydrates, including sugar, are most definitely not the cause of insulin resistance and diabetes. And, avoiding carbohydrates simply avoids the problem rather than solving it.

If you want to learn more about what actually causes type 2 diabetes and insulin resistance, check out this video. And, make sure to sign up for the free mini-course below, where you’ll learn how you can correct energy production and usage in order to improve these conditions!

References

Sugar Does NOT Cause Insulin Resistance or Diabetes

Insulin resistance is one of the main components of metabolic syndrome, which increases heart disease risk, diabetes risk, and overall mortality (1).

Diabetes and prediabetes, which are considered to be a result of insulin resistance, have reached epidemic levels. 114 million U.S. adults have diabetes or prediabetes, accounting for a staggering 35% of the entire U.S. population! (2) And the numbers are only increasing.

The worst part is that the current recommendations for handling insulin resistance and diabetes only make them worse. These recommendations center around the mistaken belief that the consumption of carbohydrates, specifically sugar, is to blame for causing and worsening these conditions.

This is a huge problem, to say the least.

What are Insulin Resistance and Diabetes?

Insulin is one of the regulators of our blood sugar.

When we consume any form of carbohydrates, including sugars, our blood sugar increases. The increase in blood sugar triggers the release of insulin, which allows sugar to move from the blood into the cells where it can be used to produce energy.

The conventional view of insulin resistance is that the cells don’t respond as well to insulin (they “resist” insulin’s effects), so the sugar isn’t moved from the blood into the cells, causing blood sugar levels to remain slightly elevated. Diabetes (type 2) is considered to be the result of a more intense form of insulin resistance, where the cells respond even less to insulin and blood sugar levels remain very high.

From this view, the problem in insulin resistance and diabetes is that sugar can’t be transported into the cells where it’s needed. But, as you’ll read in a little bit, this isn’t at all the case. In fact, insulin resistance is only a symptom of the problem.

Why Would Sugar Cause Insulin Resistance and Diabetes?

Carbohydrates, specifically sugar, are typically blamed for insulin resistance and diabetes for 2 reasons:

1. Carbohydrates increase blood sugar, which increases the secretion of insulin. It’s assumed that as our bodies secrete and use more insulin, our cells become less sensitive to it.

This idea clearly reflects the mechanical, reductionist view of the human body that permeates conventional medicine. This view focuses heavily on symptoms, and therefore has a tendency to blame the symptoms for causing the disease or condition.

In the case of insulin resistance and diabetes, this has taken the form of blaming foods that raise blood sugar and increase insulin secretion. (The same has happened with heart disease and cholesterol, as I explained here)

But, just because blood sugar increases and insulin can’t properly function in these conditions doesn’t mean that insulin resistance and diabetes are caused by too much insulin or the raising of blood sugar.

Aside from this idea being born out of the mechanical and reductionistic views of the human body, there is little evidence, if any, supporting that cells become less sensitive to insulin as they’re exposed to more insulin or higher blood sugar levels.

However, there is substantial evidence against this idea, including that high carbohydrate and sugar intakes are not associated with insulin resistance and diabetes (3, 4, 5, 6, 7). And, that increasing carbohydrate consumption actually increases insulin sensitivity (the opposite of insulin resistance) (8, 9, 10, 11, 12).

When considering that our bodies complex, adaptive systems, this isn’t surprising. Instead, it’s the expected, logical adaption to increased carbohydrate intake.

2. Carbohydrates, specifically fructose, can stimulate inflammatory pathways that cause insulin resistance.

Fructose doesn’t raise the blood sugar and increase insulin like most carbohydrates, but it’s considered the culprit for insulin resistance due to its “inflammatory and fat-producing effects.”

However, as I explained here and here, sugar, and specifically fructose, doesn’t cause inflammation and fat-production in humans unless it’s consumed in extremely large quantities (like the equivalent of 40 cans of soda over 2 days) or it isn’t being efficiently used to produce energy (we’ll talk more about this in a little bit). And, the inflammation it causes is very different from the chronic inflammation that underlies chronic diseases.

One thing that I didn’t mention in those articles is that when those inflammatory and fat-producing pathways are stimulated, they also cause insulin resistance.

But, like the “inflammation,” this insulin resistance is only temporary and doesn’t have the same consequences as the insulin resistance in metabolic syndrome and diabetes.

Instead, this temporary insulin resistance is a protective mechanism that stops more fructose from entering a liver that already has more than enough fructose. But as the liver uses this fructose, the insulin resistance dissipates.

This temporary insulin resistance is similar to the insulin resistance seen in response to low-carb and ketogenic diets, which often dissipates once the body becomes accustomed to glucose metabolism, as talked about here.

It may sound like I’m saying that not all insulin resistance is the same. And, that’s kind of true, but it would be more accurate to say that insulin resistance is only one part of the picture. The important question is why is the insulin resistance there?

It All Comes Down to Energy

As I mentioned earlier, the conventional idea that insulin resistance occurs because our cells no longer respond as well to insulin, preventing them from getting enough sugar, is a fallacy. In fact, insulin resistance isn’t the problem at all, but we’ll get to that in a second.

The problem in diabetes isn’t that the cells can’t get enough sugar, it’s that they can’t use the sugar they have to produce energy (13, 14, 15, 16). Because sugar isn’t being used to produce energy, it builds up in the cells. This blocks more sugar from entering the cells, which prevents insulin from doing its job (15).

In this situation, even giving someone extra insulin doesn’t increase the amount of sugar that enters the cells or the amount of sugar used to produce energy (13, 14, 17).

Plus, because sugar can’t enter the cells it remains in the blood, which partially accounts for the high blood sugar seen in diabetes.

And, due to the cells’ inability to use sugar to produce energy, those with diabetes have elevated levels of glucagon and cortisol, which are typically elevated under conditions of low blood sugar (or more accurately, low energy supply), despite the high blood sugar seen in diabetes (18, 19, 20).

These stress hormones cause the liver to continue to release large amounts of sugar, which is largely responsible for the high blood sugar seen in diabetes (17).

In other words, insulin resistance isn’t really the problem in diabetes! The problem is an inability to use sugar to produce energy, which inhibits the function of insulin. The lack of energy also causes high levels of glucagon and cortisol, which cause the liver to release large amounts of sugar and results in high blood sugar.

Instead of being the underlying problem, insulin resistance is simply the way that our cells say “we don’t need any more fuel.”

It can happen under conditions of extreme fructose excess or a low-carb/ketogenic diet, as was mentioned earlier. But, it’s really only a symptom of a problem when energy production is inhibited (like in diabetes), in which case the real problem is the lack of energy!

With that in mind, carbohydrates, including sugar, are most definitely not the cause of insulin resistance and diabetes. And, avoiding carbohydrates simply avoids the problem rather than solving it.

If you want to learn more about what actually causes type 2 diabetes and insulin resistance, check out this video. And, make sure to sign up for the free mini-course below, where you’ll learn how you can correct energy production and usage in order to improve these conditions!

References

Sugar Does NOT Cause Insulin Resistance or Diabetes

Insulin resistance is one of the main components of metabolic syndrome, which increases heart disease risk, diabetes risk, and overall mortality (1).

Diabetes and prediabetes, which are considered to be a result of insulin resistance, have reached epidemic levels. 114 million U.S. adults have diabetes or prediabetes, accounting for a staggering 35% of the entire U.S. population! (2) And the numbers are only increasing.

The worst part is that the current recommendations for handling insulin resistance and diabetes only make them worse. These recommendations center around the mistaken belief that the consumption of carbohydrates, specifically sugar, is to blame for causing and worsening these conditions.

This is a huge problem, to say the least.

What are Insulin Resistance and Diabetes?

Insulin is one of the regulators of our blood sugar.

When we consume any form of carbohydrates, including sugars, our blood sugar increases. The increase in blood sugar triggers the release of insulin, which allows sugar to move from the blood into the cells where it can be used to produce energy.

The conventional view of insulin resistance is that the cells don’t respond as well to insulin (they “resist” insulin’s effects), so the sugar isn’t moved from the blood into the cells, causing blood sugar levels to remain slightly elevated. Diabetes (type 2) is considered to be the result of a more intense form of insulin resistance, where the cells respond even less to insulin and blood sugar levels remain very high.

From this view, the problem in insulin resistance and diabetes is that sugar can’t be transported into the cells where it’s needed. But, as you’ll read in a little bit, this isn’t at all the case. In fact, insulin resistance is only a symptom of the problem.

Why Would Sugar Cause Insulin Resistance and Diabetes?

Carbohydrates, specifically sugar, are typically blamed for insulin resistance and diabetes for 2 reasons:

1. Carbohydrates increase blood sugar, which increases the secretion of insulin. It’s assumed that as our bodies secrete and use more insulin, our cells become less sensitive to it.

This idea clearly reflects the mechanical, reductionist view of the human body that permeates conventional medicine. This view focuses heavily on symptoms, and therefore has a tendency to blame the symptoms for causing the disease or condition.

In the case of insulin resistance and diabetes, this has taken the form of blaming foods that raise blood sugar and increase insulin secretion. (The same has happened with heart disease and cholesterol, as I explained here)

But, just because blood sugar increases and insulin can’t properly function in these conditions doesn’t mean that insulin resistance and diabetes are caused by too much insulin or the raising of blood sugar.

Aside from this idea being born out of the mechanical and reductionistic views of the human body, there is little evidence, if any, supporting that cells become less sensitive to insulin as they’re exposed to more insulin or higher blood sugar levels.

However, there is substantial evidence against this idea, including that high carbohydrate and sugar intakes are not associated with insulin resistance and diabetes (3, 4, 5, 6, 7). And, that increasing carbohydrate consumption actually increases insulin sensitivity (the opposite of insulin resistance) (8, 9, 10, 11, 12).

When considering that our bodies complex, adaptive systems, this isn’t surprising. Instead, it’s the expected, logical adaption to increased carbohydrate intake.

2. Carbohydrates, specifically fructose, can stimulate inflammatory pathways that cause insulin resistance.

Fructose doesn’t raise the blood sugar and increase insulin like most carbohydrates, but it’s considered the culprit for insulin resistance due to its “inflammatory and fat-producing effects.”

However, as I explained here and here, sugar, and specifically fructose, doesn’t cause inflammation and fat-production in humans unless it’s consumed in extremely large quantities (like the equivalent of 40 cans of soda over 2 days) or it isn’t being efficiently used to produce energy (we’ll talk more about this in a little bit). And, the inflammation it causes is very different from the chronic inflammation that underlies chronic diseases.

One thing that I didn’t mention in those articles is that when those inflammatory and fat-producing pathways are stimulated, they also cause insulin resistance.

But, like the “inflammation,” this insulin resistance is only temporary and doesn’t have the same consequences as the insulin resistance in metabolic syndrome and diabetes.

Instead, this temporary insulin resistance is a protective mechanism that stops more fructose from entering a liver that already has more than enough fructose. But as the liver uses this fructose, the insulin resistance dissipates.

This temporary insulin resistance is similar to the insulin resistance seen in response to low-carb and ketogenic diets, which often dissipates once the body becomes accustomed to glucose metabolism, as talked about here.

It may sound like I’m saying that not all insulin resistance is the same. And, that’s kind of true, but it would be more accurate to say that insulin resistance is only one part of the picture. The important question is why is the insulin resistance there?

It All Comes Down to Energy

As I mentioned earlier, the conventional idea that insulin resistance occurs because our cells no longer respond as well to insulin, preventing them from getting enough sugar, is a fallacy. In fact, insulin resistance isn’t the problem at all, but we’ll get to that in a second.

The problem in diabetes isn’t that the cells can’t get enough sugar, it’s that they can’t use the sugar they have to produce energy (13, 14, 15, 16). Because sugar isn’t being used to produce energy, it builds up in the cells. This blocks more sugar from entering the cells, which prevents insulin from doing its job (15).

In this situation, even giving someone extra insulin doesn’t increase the amount of sugar that enters the cells or the amount of sugar used to produce energy (13, 14, 17).

Plus, because sugar can’t enter the cells it remains in the blood, which partially accounts for the high blood sugar seen in diabetes.

And, due to the cells’ inability to use sugar to produce energy, those with diabetes have elevated levels of glucagon and cortisol, which are typically elevated under conditions of low blood sugar (or more accurately, low energy supply), despite the high blood sugar seen in diabetes (18, 19, 20).

These stress hormones cause the liver to continue to release large amounts of sugar, which is largely responsible for the high blood sugar seen in diabetes (17).

In other words, insulin resistance isn’t really the problem in diabetes! The problem is an inability to use sugar to produce energy, which inhibits the function of insulin. The lack of energy also causes high levels of glucagon and cortisol, which cause the liver to release large amounts of sugar and results in high blood sugar.

Instead of being the underlying problem, insulin resistance is simply the way that our cells say “we don’t need any more fuel.”

It can happen under conditions of extreme fructose excess or a low-carb/ketogenic diet, as was mentioned earlier. But, it’s really only a symptom of a problem when energy production is inhibited (like in diabetes), in which case the real problem is the lack of energy!

With that in mind, carbohydrates, including sugar, are most definitely not the cause of insulin resistance and diabetes. And, avoiding carbohydrates simply avoids the problem rather than solving it.

If you want to learn more about what actually causes type 2 diabetes and insulin resistance, check out this video. And, make sure to sign up for the free mini-course below, where you’ll learn how you can correct energy production and usage in order to improve these conditions!

References

Sugar Does NOT Cause Insulin Resistance or Diabetes

Insulin resistance is one of the main components of metabolic syndrome, which increases heart disease risk, diabetes risk, and overall mortality (1).

Diabetes and prediabetes, which are considered to be a result of insulin resistance, have reached epidemic levels. 114 million U.S. adults have diabetes or prediabetes, accounting for a staggering 35% of the entire U.S. population! (2) And the numbers are only increasing.

The worst part is that the current recommendations for handling insulin resistance and diabetes only make them worse. These recommendations center around the mistaken belief that the consumption of carbohydrates, specifically sugar, is to blame for causing and worsening these conditions.

This is a huge problem, to say the least.

What are Insulin Resistance and Diabetes?

Insulin is one of the regulators of our blood sugar.

When we consume any form of carbohydrates, including sugars, our blood sugar increases. The increase in blood sugar triggers the release of insulin, which allows sugar to move from the blood into the cells where it can be used to produce energy.

The conventional view of insulin resistance is that the cells don’t respond as well to insulin (they “resist” insulin’s effects), so the sugar isn’t moved from the blood into the cells, causing blood sugar levels to remain slightly elevated. Diabetes (type 2) is considered to be the result of a more intense form of insulin resistance, where the cells respond even less to insulin and blood sugar levels remain very high.

From this view, the problem in insulin resistance and diabetes is that sugar can’t be transported into the cells where it’s needed. But, as you’ll read in a little bit, this isn’t at all the case. In fact, insulin resistance is only a symptom of the problem.

Why Would Sugar Cause Insulin Resistance and Diabetes?

Carbohydrates, specifically sugar, are typically blamed for insulin resistance and diabetes for 2 reasons:

1. Carbohydrates increase blood sugar, which increases the secretion of insulin. It’s assumed that as our bodies secrete and use more insulin, our cells become less sensitive to it.

This idea clearly reflects the mechanical, reductionist view of the human body that permeates conventional medicine. This view focuses heavily on symptoms, and therefore has a tendency to blame the symptoms for causing the disease or condition.

In the case of insulin resistance and diabetes, this has taken the form of blaming foods that raise blood sugar and increase insulin secretion. (The same has happened with heart disease and cholesterol, as I explained here)

But, just because blood sugar increases and insulin can’t properly function in these conditions doesn’t mean that insulin resistance and diabetes are caused by too much insulin or the raising of blood sugar.

Aside from this idea being born out of the mechanical and reductionistic views of the human body, there is little evidence, if any, supporting that cells become less sensitive to insulin as they’re exposed to more insulin or higher blood sugar levels.

However, there is substantial evidence against this idea, including that high carbohydrate and sugar intakes are not associated with insulin resistance and diabetes (3, 4, 5, 6, 7). And, that increasing carbohydrate consumption actually increases insulin sensitivity (the opposite of insulin resistance) (8, 9, 10, 11, 12).

When considering that our bodies complex, adaptive systems, this isn’t surprising. Instead, it’s the expected, logical adaption to increased carbohydrate intake.

2. Carbohydrates, specifically fructose, can stimulate inflammatory pathways that cause insulin resistance.

Fructose doesn’t raise the blood sugar and increase insulin like most carbohydrates, but it’s considered the culprit for insulin resistance due to its “inflammatory and fat-producing effects.”

However, as I explained here and here, sugar, and specifically fructose, doesn’t cause inflammation and fat-production in humans unless it’s consumed in extremely large quantities (like the equivalent of 40 cans of soda over 2 days) or it isn’t being efficiently used to produce energy (we’ll talk more about this in a little bit). And, the inflammation it causes is very different from the chronic inflammation that underlies chronic diseases.

One thing that I didn’t mention in those articles is that when those inflammatory and fat-producing pathways are stimulated, they also cause insulin resistance.

But, like the “inflammation,” this insulin resistance is only temporary and doesn’t have the same consequences as the insulin resistance in metabolic syndrome and diabetes.

Instead, this temporary insulin resistance is a protective mechanism that stops more fructose from entering a liver that already has more than enough fructose. But as the liver uses this fructose, the insulin resistance dissipates.

This temporary insulin resistance is similar to the insulin resistance seen in response to low-carb and ketogenic diets, which often dissipates once the body becomes accustomed to glucose metabolism, as talked about here.

It may sound like I’m saying that not all insulin resistance is the same. And, that’s kind of true, but it would be more accurate to say that insulin resistance is only one part of the picture. The important question is why is the insulin resistance there?

It All Comes Down to Energy

As I mentioned earlier, the conventional idea that insulin resistance occurs because our cells no longer respond as well to insulin, preventing them from getting enough sugar, is a fallacy. In fact, insulin resistance isn’t the problem at all, but we’ll get to that in a second.

The problem in diabetes isn’t that the cells can’t get enough sugar, it’s that they can’t use the sugar they have to produce energy (13, 14, 15, 16). Because sugar isn’t being used to produce energy, it builds up in the cells. This blocks more sugar from entering the cells, which prevents insulin from doing its job (15).

In this situation, even giving someone extra insulin doesn’t increase the amount of sugar that enters the cells or the amount of sugar used to produce energy (13, 14, 17).

Plus, because sugar can’t enter the cells it remains in the blood, which partially accounts for the high blood sugar seen in diabetes.

And, due to the cells’ inability to use sugar to produce energy, those with diabetes have elevated levels of glucagon and cortisol, which are typically elevated under conditions of low blood sugar (or more accurately, low energy supply), despite the high blood sugar seen in diabetes (18, 19, 20).

These stress hormones cause the liver to continue to release large amounts of sugar, which is largely responsible for the high blood sugar seen in diabetes (17).

In other words, insulin resistance isn’t really the problem in diabetes! The problem is an inability to use sugar to produce energy, which inhibits the function of insulin. The lack of energy also causes high levels of glucagon and cortisol, which cause the liver to release large amounts of sugar and results in high blood sugar.

Instead of being the underlying problem, insulin resistance is simply the way that our cells say “we don’t need any more fuel.”

It can happen under conditions of extreme fructose excess or a low-carb/ketogenic diet, as was mentioned earlier. But, it’s really only a symptom of a problem when energy production is inhibited (like in diabetes), in which case the real problem is the lack of energy!

With that in mind, carbohydrates, including sugar, are most definitely not the cause of insulin resistance and diabetes. And, avoiding carbohydrates simply avoids the problem rather than solving it.

If you want to learn more about what actually causes type 2 diabetes and insulin resistance, check out this video. And, make sure to sign up for the free mini-course below, where you’ll learn how you can correct energy production and usage in order to improve these conditions!

References

Sugar Does NOT Cause Insulin Resistance or Diabetes

Insulin resistance is one of the main components of metabolic syndrome, which increases heart disease risk, diabetes risk, and overall mortality (1).

Diabetes and prediabetes, which are considered to be a result of insulin resistance, have reached epidemic levels. 114 million U.S. adults have diabetes or prediabetes, accounting for a staggering 35% of the entire U.S. population! (2) And the numbers are only increasing.

The worst part is that the current recommendations for handling insulin resistance and diabetes only make them worse. These recommendations center around the mistaken belief that the consumption of carbohydrates, specifically sugar, is to blame for causing and worsening these conditions.

This is a huge problem, to say the least.

What are Insulin Resistance and Diabetes?

Insulin is one of the regulators of our blood sugar.

When we consume any form of carbohydrates, including sugars, our blood sugar increases. The increase in blood sugar triggers the release of insulin, which allows sugar to move from the blood into the cells where it can be used to produce energy.

The conventional view of insulin resistance is that the cells don’t respond as well to insulin (they “resist” insulin’s effects), so the sugar isn’t moved from the blood into the cells, causing blood sugar levels to remain slightly elevated. Diabetes (type 2) is considered to be the result of a more intense form of insulin resistance, where the cells respond even less to insulin and blood sugar levels remain very high.

From this view, the problem in insulin resistance and diabetes is that sugar can’t be transported into the cells where it’s needed. But, as you’ll read in a little bit, this isn’t at all the case. In fact, insulin resistance is only a symptom of the problem.

Why Would Sugar Cause Insulin Resistance and Diabetes?

Carbohydrates, specifically sugar, are typically blamed for insulin resistance and diabetes for 2 reasons:

1. Carbohydrates increase blood sugar, which increases the secretion of insulin. It’s assumed that as our bodies secrete and use more insulin, our cells become less sensitive to it.

This idea clearly reflects the mechanical, reductionist view of the human body that permeates conventional medicine. This view focuses heavily on symptoms, and therefore has a tendency to blame the symptoms for causing the disease or condition.

In the case of insulin resistance and diabetes, this has taken the form of blaming foods that raise blood sugar and increase insulin secretion. (The same has happened with heart disease and cholesterol, as I explained here)

But, just because blood sugar increases and insulin can’t properly function in these conditions doesn’t mean that insulin resistance and diabetes are caused by too much insulin or the raising of blood sugar.

Aside from this idea being born out of the mechanical and reductionistic views of the human body, there is little evidence, if any, supporting that cells become less sensitive to insulin as they’re exposed to more insulin or higher blood sugar levels.

However, there is substantial evidence against this idea, including that high carbohydrate and sugar intakes are not associated with insulin resistance and diabetes (3, 4, 5, 6, 7). And, that increasing carbohydrate consumption actually increases insulin sensitivity (the opposite of insulin resistance) (8, 9, 10, 11, 12).

When considering that our bodies complex, adaptive systems, this isn’t surprising. Instead, it’s the expected, logical adaption to increased carbohydrate intake.

2. Carbohydrates, specifically fructose, can stimulate inflammatory pathways that cause insulin resistance.

Fructose doesn’t raise the blood sugar and increase insulin like most carbohydrates, but it’s considered the culprit for insulin resistance due to its “inflammatory and fat-producing effects.”

However, as I explained here and here, sugar, and specifically fructose, doesn’t cause inflammation and fat-production in humans unless it’s consumed in extremely large quantities (like the equivalent of 40 cans of soda over 2 days) or it isn’t being efficiently used to produce energy (we’ll talk more about this in a little bit). And, the inflammation it causes is very different from the chronic inflammation that underlies chronic diseases.

One thing that I didn’t mention in those articles is that when those inflammatory and fat-producing pathways are stimulated, they also cause insulin resistance.

But, like the “inflammation,” this insulin resistance is only temporary and doesn’t have the same consequences as the insulin resistance in metabolic syndrome and diabetes.

Instead, this temporary insulin resistance is a protective mechanism that stops more fructose from entering a liver that already has more than enough fructose. But as the liver uses this fructose, the insulin resistance dissipates.

This temporary insulin resistance is similar to the insulin resistance seen in response to low-carb and ketogenic diets, which often dissipates once the body becomes accustomed to glucose metabolism, as talked about here.

It may sound like I’m saying that not all insulin resistance is the same. And, that’s kind of true, but it would be more accurate to say that insulin resistance is only one part of the picture. The important question is why is the insulin resistance there?

It All Comes Down to Energy

As I mentioned earlier, the conventional idea that insulin resistance occurs because our cells no longer respond as well to insulin, preventing them from getting enough sugar, is a fallacy. In fact, insulin resistance isn’t the problem at all, but we’ll get to that in a second.

The problem in diabetes isn’t that the cells can’t get enough sugar, it’s that they can’t use the sugar they have to produce energy (13, 14, 15, 16). Because sugar isn’t being used to produce energy, it builds up in the cells. This blocks more sugar from entering the cells, which prevents insulin from doing its job (15).

In this situation, even giving someone extra insulin doesn’t increase the amount of sugar that enters the cells or the amount of sugar used to produce energy (13, 14, 17).

Plus, because sugar can’t enter the cells it remains in the blood, which partially accounts for the high blood sugar seen in diabetes.

And, due to the cells’ inability to use sugar to produce energy, those with diabetes have elevated levels of glucagon and cortisol, which are typically elevated under conditions of low blood sugar (or more accurately, low energy supply), despite the high blood sugar seen in diabetes (18, 19, 20).

These stress hormones cause the liver to continue to release large amounts of sugar, which is largely responsible for the high blood sugar seen in diabetes (17).

In other words, insulin resistance isn’t really the problem in diabetes! The problem is an inability to use sugar to produce energy, which inhibits the function of insulin. The lack of energy also causes high levels of glucagon and cortisol, which cause the liver to release large amounts of sugar and results in high blood sugar.

Instead of being the underlying problem, insulin resistance is simply the way that our cells say “we don’t need any more fuel.”

It can happen under conditions of extreme fructose excess or a low-carb/ketogenic diet, as was mentioned earlier. But, it’s really only a symptom of a problem when energy production is inhibited (like in diabetes), in which case the real problem is the lack of energy!

With that in mind, carbohydrates, including sugar, are most definitely not the cause of insulin resistance and diabetes. And, avoiding carbohydrates simply avoids the problem rather than solving it.

If you want to learn more about what actually causes type 2 diabetes and insulin resistance, check out this video. And, make sure to sign up for the free mini-course below, where you’ll learn how you can correct energy production and usage in order to improve these conditions!

References

Sugar Does NOT Cause Insulin Resistance or Diabetes

Insulin resistance is one of the main components of metabolic syndrome, which increases heart disease risk, diabetes risk, and overall mortality (1).

Diabetes and prediabetes, which are considered to be a result of insulin resistance, have reached epidemic levels. 114 million U.S. adults have diabetes or prediabetes, accounting for a staggering 35% of the entire U.S. population! (2) And the numbers are only increasing.

The worst part is that the current recommendations for handling insulin resistance and diabetes only make them worse. These recommendations center around the mistaken belief that the consumption of carbohydrates, specifically sugar, is to blame for causing and worsening these conditions.

This is a huge problem, to say the least.

What are Insulin Resistance and Diabetes?

Insulin is one of the regulators of our blood sugar.

When we consume any form of carbohydrates, including sugars, our blood sugar increases. The increase in blood sugar triggers the release of insulin, which allows sugar to move from the blood into the cells where it can be used to produce energy.

The conventional view of insulin resistance is that the cells don’t respond as well to insulin (they “resist” insulin’s effects), so the sugar isn’t moved from the blood into the cells, causing blood sugar levels to remain slightly elevated. Diabetes (type 2) is considered to be the result of a more intense form of insulin resistance, where the cells respond even less to insulin and blood sugar levels remain very high.

From this view, the problem in insulin resistance and diabetes is that sugar can’t be transported into the cells where it’s needed. But, as you’ll read in a little bit, this isn’t at all the case. In fact, insulin resistance is only a symptom of the problem.

Why Would Sugar Cause Insulin Resistance and Diabetes?

Carbohydrates, specifically sugar, are typically blamed for insulin resistance and diabetes for 2 reasons:

1. Carbohydrates increase blood sugar, which increases the secretion of insulin. It’s assumed that as our bodies secrete and use more insulin, our cells become less sensitive to it.

This idea clearly reflects the mechanical, reductionist view of the human body that permeates conventional medicine. This view focuses heavily on symptoms, and therefore has a tendency to blame the symptoms for causing the disease or condition.

In the case of insulin resistance and diabetes, this has taken the form of blaming foods that raise blood sugar and increase insulin secretion. (The same has happened with heart disease and cholesterol, as I explained here)

But, just because blood sugar increases and insulin can’t properly function in these conditions doesn’t mean that insulin resistance and diabetes are caused by too much insulin or the raising of blood sugar.

Aside from this idea being born out of the mechanical and reductionistic views of the human body, there is little evidence, if any, supporting that cells become less sensitive to insulin as they’re exposed to more insulin or higher blood sugar levels.

However, there is substantial evidence against this idea, including that high carbohydrate and sugar intakes are not associated with insulin resistance and diabetes (3, 4, 5, 6, 7). And, that increasing carbohydrate consumption actually increases insulin sensitivity (the opposite of insulin resistance) (8, 9, 10, 11, 12).

When considering that our bodies complex, adaptive systems, this isn’t surprising. Instead, it’s the expected, logical adaption to increased carbohydrate intake.

2. Carbohydrates, specifically fructose, can stimulate inflammatory pathways that cause insulin resistance.

Fructose doesn’t raise the blood sugar and increase insulin like most carbohydrates, but it’s considered the culprit for insulin resistance due to its “inflammatory and fat-producing effects.”

However, as I explained here and here, sugar, and specifically fructose, doesn’t cause inflammation and fat-production in humans unless it’s consumed in extremely large quantities (like the equivalent of 40 cans of soda over 2 days) or it isn’t being efficiently used to produce energy (we’ll talk more about this in a little bit). And, the inflammation it causes is very different from the chronic inflammation that underlies chronic diseases.

One thing that I didn’t mention in those articles is that when those inflammatory and fat-producing pathways are stimulated, they also cause insulin resistance.

But, like the “inflammation,” this insulin resistance is only temporary and doesn’t have the same consequences as the insulin resistance in metabolic syndrome and diabetes.

Instead, this temporary insulin resistance is a protective mechanism that stops more fructose from entering a liver that already has more than enough fructose. But as the liver uses this fructose, the insulin resistance dissipates.

This temporary insulin resistance is similar to the insulin resistance seen in response to low-carb and ketogenic diets, which often dissipates once the body becomes accustomed to glucose metabolism, as talked about here.

It may sound like I’m saying that not all insulin resistance is the same. And, that’s kind of true, but it would be more accurate to say that insulin resistance is only one part of the picture. The important question is why is the insulin resistance there?

It All Comes Down to Energy

As I mentioned earlier, the conventional idea that insulin resistance occurs because our cells no longer respond as well to insulin, preventing them from getting enough sugar, is a fallacy. In fact, insulin resistance isn’t the problem at all, but we’ll get to that in a second.

The problem in diabetes isn’t that the cells can’t get enough sugar, it’s that they can’t use the sugar they have to produce energy (13, 14, 15, 16). Because sugar isn’t being used to produce energy, it builds up in the cells. This blocks more sugar from entering the cells, which prevents insulin from doing its job (15).

In this situation, even giving someone extra insulin doesn’t increase the amount of sugar that enters the cells or the amount of sugar used to produce energy (13, 14, 17).

Plus, because sugar can’t enter the cells it remains in the blood, which partially accounts for the high blood sugar seen in diabetes.

And, due to the cells’ inability to use sugar to produce energy, those with diabetes have elevated levels of glucagon and cortisol, which are typically elevated under conditions of low blood sugar (or more accurately, low energy supply), despite the high blood sugar seen in diabetes (18, 19, 20).

These stress hormones cause the liver to continue to release large amounts of sugar, which is largely responsible for the high blood sugar seen in diabetes (17).

In other words, insulin resistance isn’t really the problem in diabetes! The problem is an inability to use sugar to produce energy, which inhibits the function of insulin. The lack of energy also causes high levels of glucagon and cortisol, which cause the liver to release large amounts of sugar and results in high blood sugar.

Instead of being the underlying problem, insulin resistance is simply the way that our cells say “we don’t need any more fuel.”

It can happen under conditions of extreme fructose excess or a low-carb/ketogenic diet, as was mentioned earlier. But, it’s really only a symptom of a problem when energy production is inhibited (like in diabetes), in which case the real problem is the lack of energy!

With that in mind, carbohydrates, including sugar, are most definitely not the cause of insulin resistance and diabetes. And, avoiding carbohydrates simply avoids the problem rather than solving it.

If you want to learn more about what actually causes type 2 diabetes and insulin resistance, check out this video. And, make sure to sign up for the free mini-course below, where you’ll learn how you can correct energy production and usage in order to improve these conditions!

References

The Cholesterol Nonsense Continues

I really thought we were done with all the anti-cholesterol nonsense, but it just won’t go away.

The anti-cholesterol narrative has been thoroughly discredited over the past couple decades, and even the Dietary Guidelines for Americans has removed their previous dietary limits for cholesterol consumption due to a lack of supporting evidence (although they still suggest consuming as little cholesterol as possible) (1).

But, most people are still avoiding cholesterol-containing foods like eggs and red meat, and the incredibly harmful and dangerous cholesterol-lowering drugs are still the most prescribed drugs in the United States (2).

The anti-cholesterol story began with the notion that high blood cholesterol levels cause plaque formation, which causes heart attacks. This led to the recommendations to reduce dietary cholesterol, which are still pervasive today.

But, not only does cholesterol not cause plaque formation or heart attacks, it actually protects against them and is one of the most protective nutrients available to our bodies.

 

Cholesterol Does NOT Cause Heart Disease

Efforts to link cholesterol to heart disease have gone on for half a century and have failed miserably.

Well, I guess it depends how you define “failed,” considering the amount of cholesterol-lowering drugs sold and the persistence of the anti-cholesterol dietary advice. But as far as scientific evidence goes, they have certainly failed.

The most influential heart disease study ever done found that the cholesterol levels between those who developed heart disease and those who didn’t were nearly identical (3).

This hardly supports that cholesterol causes heart disease, and many other studies have found that people with higher levels of cholesterol are less likely to die from heart disease and that those with heart disease who have higher cholesterol levels are less likely to die from any cause (4, 5, 6, 7, 8).

This is not to mention that the amount of cholesterol we eat doesn’t affect our blood levels of cholesterol or our risk of heart disease! (9, 10) Our bodies produce their own cholesterol, so the amount of cholesterol we consume has little effect on the amount of cholesterol in our bodies.

In fact, our bodies use between 1,000 and 2,000 mg of cholesterol per day, and if we reduce the amount of cholesterol we consume then our bodies simply make more in response.

So, not only do the cholesterol levels in our blood not cause heart disease, eating high-cholesterol foods doesn’t increase those levels anyway!

But what about the plaques that form in our arteries and cause heart attacks? Aren’t they made up of cholesterol?

Yeah, partially. But, blaming cholesterol for the plaque is kind of like blaming firemen for a fire.

As you’ll read about in a little bit, cholesterol is a vital part of our immune system. So, while it is found in atherosclerotic plaques, it’s there as a protective factor rather than a cause (11). Polyunsaturated fats (PUFA) and their metabolites, on the other hand, are also found in these plaques and play a more causative role by contributing to oxidation and inflammation (12, 13, 14, 15).

But, while cholesterol levels, plaque, and heart disease aren’t affected by the amount of cholesterol we eat, they are directly affected by our metabolism.

 

Cholesterol and Metabolism

Cholesterol levels are influenced by many different variables, but the factor that has the largest effect is metabolism. This relationship between cholesterol and metabolism has been known for 100 years but is now largely ignored (16, 17, 18).

When our metabolism is high, we produce more cholesterol. But, we also use more cholesterol to produce the protective steroid hormones (and for other uses), which reduces the amount of cholesterol in our blood (18).

The opposite occurs when our metabolism is low. We produce less cholesterol and use less of it to produce the protective hormones, leaving more of it in the blood (18).

So, while the larger amount of cholesterol in the blood isn’t a problem on its own, it’s representative of a low metabolism, which is a problem and is associated with heart disease (19, 20). Plus, it means the body is using less cholesterol, which is also a problem due to cholesterol’s beneficial effects.

 

The Protective Effects of Cholesterol

Cholesterol is one of the most protective nutrients that exist in our bodies. It’s vital for brain function, immune function, and digestion, and is the precursor to the extremely important steroid hormones.

Our brains contain around 25% of all the cholesterol in our bodies because of its importance in brain function (21). And, a lack of cholesterol is associated with impaired cognitive function as well as depression and impaired mental health (22, 23).

Cholesterol also plays a major role in our immune system and is able to prevent infections and detoxify harmful toxins like endotoxin (11, 24, 25).

And, due to cholesterol’s protective effects, low cholesterol and cholesterol-lowering drugs have been shown to increase the risk of cancer and all-cause mortality (26, 27).

In other words, we can stop with the anti-cholesterol nonsense!

We NEED cholesterol and we don’t need to avoid foods that contain it (like eggs and other animal foods) or that increase our bodies production of it (like sugar and saturated fat). In fact, the cholesterol-producing and metabolism-supporting effects of these foods make them some of the best foods for supporting health.

If you have high cholesterol then a low metabolism is to blame, not these foods, and a cholesterol-lowering drug is not the answer.

 

References

The Cholesterol Nonsense Continues

I really thought we were done with all the anti-cholesterol nonsense, but it just won’t go away.

The anti-cholesterol narrative has been thoroughly discredited over the past couple decades, and even the Dietary Guidelines for Americans has removed their previous dietary limits for cholesterol consumption due to a lack of supporting evidence (although they still suggest consuming as little cholesterol as possible) (1).

But, most people are still avoiding cholesterol-containing foods like eggs and red meat, and the incredibly harmful and dangerous cholesterol-lowering drugs are still the most prescribed drugs in the United States (2).

The anti-cholesterol story began with the notion that high blood cholesterol levels cause plaque formation, which causes heart attacks. This led to the recommendations to reduce dietary cholesterol, which are still pervasive today.

But, not only does cholesterol not cause plaque formation or heart attacks, it actually protects against them and is one of the most protective nutrients available to our bodies.

 

Cholesterol Does NOT Cause Heart Disease

Efforts to link cholesterol to heart disease have gone on for half a century and have failed miserably.

Well, I guess it depends how you define “failed,” considering the amount of cholesterol-lowering drugs sold and the persistence of the anti-cholesterol dietary advice. But as far as scientific evidence goes, they have certainly failed.

The most influential heart disease study ever done found that the cholesterol levels between those who developed heart disease and those who didn’t were nearly identical (3).

This hardly supports that cholesterol causes heart disease, and many other studies have found that people with higher levels of cholesterol are less likely to die from heart disease and that those with heart disease who have higher cholesterol levels are less likely to die from any cause (4, 5, 6, 7, 8).

This is not to mention that the amount of cholesterol we eat doesn’t affect our blood levels of cholesterol or our risk of heart disease! (9, 10) Our bodies produce their own cholesterol, so the amount of cholesterol we consume has little effect on the amount of cholesterol in our bodies.

In fact, our bodies use between 1,000 and 2,000 mg of cholesterol per day, and if we reduce the amount of cholesterol we consume then our bodies simply make more in response.

So, not only do the cholesterol levels in our blood not cause heart disease, eating high-cholesterol foods doesn’t increase those levels anyway!

But what about the plaques that form in our arteries and cause heart attacks? Aren’t they made up of cholesterol?

Yeah, partially. But, blaming cholesterol for the plaque is kind of like blaming firemen for a fire.

As you’ll read about in a little bit, cholesterol is a vital part of our immune system. So, while it is found in atherosclerotic plaques, it’s there as a protective factor rather than a cause (11). Polyunsaturated fats (PUFA) and their metabolites, on the other hand, are also found in these plaques and play a more causative role by contributing to oxidation and inflammation (12, 13, 14, 15).

But, while cholesterol levels, plaque, and heart disease aren’t affected by the amount of cholesterol we eat, they are directly affected by our metabolism.

 

Cholesterol and Metabolism

Cholesterol levels are influenced by many different variables, but the factor that has the largest effect is metabolism. This relationship between cholesterol and metabolism has been known for 100 years but is now largely ignored (16, 17, 18).

When our metabolism is high, we produce more cholesterol. But, we also use more cholesterol to produce the protective steroid hormones (and for other uses), which reduces the amount of cholesterol in our blood (18).

The opposite occurs when our metabolism is low. We produce less cholesterol and use less of it to produce the protective hormones, leaving more of it in the blood (18).

So, while the larger amount of cholesterol in the blood isn’t a problem on its own, it’s representative of a low metabolism, which is a problem and is associated with heart disease (19, 20). Plus, it means the body is using less cholesterol, which is also a problem due to cholesterol’s beneficial effects.

 

The Protective Effects of Cholesterol

Cholesterol is one of the most protective nutrients that exist in our bodies. It’s vital for brain function, immune function, and digestion, and is the precursor to the extremely important steroid hormones.

Our brains contain around 25% of all the cholesterol in our bodies because of its importance in brain function (21). And, a lack of cholesterol is associated with impaired cognitive function as well as depression and impaired mental health (22, 23).

Cholesterol also plays a major role in our immune system and is able to prevent infections and detoxify harmful toxins like endotoxin (11, 24, 25).

And, due to cholesterol’s protective effects, low cholesterol and cholesterol-lowering drugs have been shown to increase the risk of cancer and all-cause mortality (26, 27).

In other words, we can stop with the anti-cholesterol nonsense!

We NEED cholesterol and we don’t need to avoid foods that contain it (like eggs and other animal foods) or that increase our bodies production of it (like sugar and saturated fat). In fact, the cholesterol-producing and metabolism-supporting effects of these foods make them some of the best foods for supporting health.

If you have high cholesterol then a low metabolism is to blame, not these foods, and a cholesterol-lowering drug is not the answer.

 

References

The Cholesterol Nonsense Continues

I really thought we were done with all the anti-cholesterol nonsense, but it just won’t go away.

The anti-cholesterol narrative has been thoroughly discredited over the past couple decades, and even the Dietary Guidelines for Americans has removed their previous dietary limits for cholesterol consumption due to a lack of supporting evidence (although they still suggest consuming as little cholesterol as possible) (1).

But, most people are still avoiding cholesterol-containing foods like eggs and red meat, and the incredibly harmful and dangerous cholesterol-lowering drugs are still the most prescribed drugs in the United States (2).

The anti-cholesterol story began with the notion that high blood cholesterol levels cause plaque formation, which causes heart attacks. This led to the recommendations to reduce dietary cholesterol, which are still pervasive today.

But, not only does cholesterol not cause plaque formation or heart attacks, it actually protects against them and is one of the most protective nutrients available to our bodies.

 

Cholesterol Does NOT Cause Heart Disease

Efforts to link cholesterol to heart disease have gone on for half a century and have failed miserably.

Well, I guess it depends how you define “failed,” considering the amount of cholesterol-lowering drugs sold and the persistence of the anti-cholesterol dietary advice. But as far as scientific evidence goes, they have certainly failed.

The most influential heart disease study ever done found that the cholesterol levels between those who developed heart disease and those who didn’t were nearly identical (3).

This hardly supports that cholesterol causes heart disease, and many other studies have found that people with higher levels of cholesterol are less likely to die from heart disease and that those with heart disease who have higher cholesterol levels are less likely to die from any cause (4, 5, 6, 7, 8).

This is not to mention that the amount of cholesterol we eat doesn’t affect our blood levels of cholesterol or our risk of heart disease! (9, 10) Our bodies produce their own cholesterol, so the amount of cholesterol we consume has little effect on the amount of cholesterol in our bodies.

In fact, our bodies use between 1,000 and 2,000 mg of cholesterol per day, and if we reduce the amount of cholesterol we consume then our bodies simply make more in response.

So, not only do the cholesterol levels in our blood not cause heart disease, eating high-cholesterol foods doesn’t increase those levels anyway!

But what about the plaques that form in our arteries and cause heart attacks? Aren’t they made up of cholesterol?

Yeah, partially. But, blaming cholesterol for the plaque is kind of like blaming firemen for a fire.

As you’ll read about in a little bit, cholesterol is a vital part of our immune system. So, while it is found in atherosclerotic plaques, it’s there as a protective factor rather than a cause (11). Polyunsaturated fats (PUFA) and their metabolites, on the other hand, are also found in these plaques and play a more causative role by contributing to oxidation and inflammation (12, 13, 14, 15).

But, while cholesterol levels, plaque, and heart disease aren’t affected by the amount of cholesterol we eat, they are directly affected by our metabolism.

 

Cholesterol and Metabolism

Cholesterol levels are influenced by many different variables, but the factor that has the largest effect is metabolism. This relationship between cholesterol and metabolism has been known for 100 years but is now largely ignored (16, 17, 18).

When our metabolism is high, we produce more cholesterol. But, we also use more cholesterol to produce the protective steroid hormones (and for other uses), which reduces the amount of cholesterol in our blood (18).

The opposite occurs when our metabolism is low. We produce less cholesterol and use less of it to produce the protective hormones, leaving more of it in the blood (18).

So, while the larger amount of cholesterol in the blood isn’t a problem on its own, it’s representative of a low metabolism, which is a problem and is associated with heart disease (19, 20). Plus, it means the body is using less cholesterol, which is also a problem due to cholesterol’s beneficial effects.

 

The Protective Effects of Cholesterol

Cholesterol is one of the most protective nutrients that exist in our bodies. It’s vital for brain function, immune function, and digestion, and is the precursor to the extremely important steroid hormones.

Our brains contain around 25% of all the cholesterol in our bodies because of its importance in brain function (21). And, a lack of cholesterol is associated with impaired cognitive function as well as depression and impaired mental health (22, 23).

Cholesterol also plays a major role in our immune system and is able to prevent infections and detoxify harmful toxins like endotoxin (11, 24, 25).

And, due to cholesterol’s protective effects, low cholesterol and cholesterol-lowering drugs have been shown to increase the risk of cancer and all-cause mortality (26, 27).

In other words, we can stop with the anti-cholesterol nonsense!

We NEED cholesterol and we don’t need to avoid foods that contain it (like eggs and other animal foods) or that increase our bodies production of it (like sugar and saturated fat). In fact, the cholesterol-producing and metabolism-supporting effects of these foods make them some of the best foods for supporting health.

If you have high cholesterol then a low metabolism is to blame, not these foods, and a cholesterol-lowering drug is not the answer.

 

References

The Cholesterol Nonsense Continues

I really thought we were done with all the anti-cholesterol nonsense, but it just won’t go away.

The anti-cholesterol narrative has been thoroughly discredited over the past couple decades, and even the Dietary Guidelines for Americans has removed their previous dietary limits for cholesterol consumption due to a lack of supporting evidence (although they still suggest consuming as little cholesterol as possible) (1).

But, most people are still avoiding cholesterol-containing foods like eggs and red meat, and the incredibly harmful and dangerous cholesterol-lowering drugs are still the most prescribed drugs in the United States (2).

The anti-cholesterol story began with the notion that high blood cholesterol levels cause plaque formation, which causes heart attacks. This led to the recommendations to reduce dietary cholesterol, which are still pervasive today.

But, not only does cholesterol not cause plaque formation or heart attacks, it actually protects against them and is one of the most protective nutrients available to our bodies.

 

Cholesterol Does NOT Cause Heart Disease

Efforts to link cholesterol to heart disease have gone on for half a century and have failed miserably.

Well, I guess it depends how you define “failed,” considering the amount of cholesterol-lowering drugs sold and the persistence of the anti-cholesterol dietary advice. But as far as scientific evidence goes, they have certainly failed.

The most influential heart disease study ever done found that the cholesterol levels between those who developed heart disease and those who didn’t were nearly identical (3).

This hardly supports that cholesterol causes heart disease, and many other studies have found that people with higher levels of cholesterol are less likely to die from heart disease and that those with heart disease who have higher cholesterol levels are less likely to die from any cause (4, 5, 6, 7, 8).

This is not to mention that the amount of cholesterol we eat doesn’t affect our blood levels of cholesterol or our risk of heart disease! (9, 10) Our bodies produce their own cholesterol, so the amount of cholesterol we consume has little effect on the amount of cholesterol in our bodies.

In fact, our bodies use between 1,000 and 2,000 mg of cholesterol per day, and if we reduce the amount of cholesterol we consume then our bodies simply make more in response.

So, not only do the cholesterol levels in our blood not cause heart disease, eating high-cholesterol foods doesn’t increase those levels anyway!

But what about the plaques that form in our arteries and cause heart attacks? Aren’t they made up of cholesterol?

Yeah, partially. But, blaming cholesterol for the plaque is kind of like blaming firemen for a fire.

As you’ll read about in a little bit, cholesterol is a vital part of our immune system. So, while it is found in atherosclerotic plaques, it’s there as a protective factor rather than a cause (11). Polyunsaturated fats (PUFA) and their metabolites, on the other hand, are also found in these plaques and play a more causative role by contributing to oxidation and inflammation (12, 13, 14, 15).

But, while cholesterol levels, plaque, and heart disease aren’t affected by the amount of cholesterol we eat, they are directly affected by our metabolism.

 

Cholesterol and Metabolism

Cholesterol levels are influenced by many different variables, but the factor that has the largest effect is metabolism. This relationship between cholesterol and metabolism has been known for 100 years but is now largely ignored (16, 17, 18).

When our metabolism is high, we produce more cholesterol. But, we also use more cholesterol to produce the protective steroid hormones (and for other uses), which reduces the amount of cholesterol in our blood (18).

The opposite occurs when our metabolism is low. We produce less cholesterol and use less of it to produce the protective hormones, leaving more of it in the blood (18).

So, while the larger amount of cholesterol in the blood isn’t a problem on its own, it’s representative of a low metabolism, which is a problem and is associated with heart disease (19, 20). Plus, it means the body is using less cholesterol, which is also a problem due to cholesterol’s beneficial effects.

 

The Protective Effects of Cholesterol

Cholesterol is one of the most protective nutrients that exist in our bodies. It’s vital for brain function, immune function, and digestion, and is the precursor to the extremely important steroid hormones.

Our brains contain around 25% of all the cholesterol in our bodies because of its importance in brain function (21). And, a lack of cholesterol is associated with impaired cognitive function as well as depression and impaired mental health (22, 23).

Cholesterol also plays a major role in our immune system and is able to prevent infections and detoxify harmful toxins like endotoxin (11, 24, 25).

And, due to cholesterol’s protective effects, low cholesterol and cholesterol-lowering drugs have been shown to increase the risk of cancer and all-cause mortality (26, 27).

In other words, we can stop with the anti-cholesterol nonsense!

We NEED cholesterol and we don’t need to avoid foods that contain it (like eggs and other animal foods) or that increase our bodies production of it (like sugar and saturated fat). In fact, the cholesterol-producing and metabolism-supporting effects of these foods make them some of the best foods for supporting health.

If you have high cholesterol then a low metabolism is to blame, not these foods, and a cholesterol-lowering drug is not the answer.

 

References

The Cholesterol Nonsense Continues

I really thought we were done with all the anti-cholesterol nonsense, but it just won’t go away.

The anti-cholesterol narrative has been thoroughly discredited over the past couple decades, and even the Dietary Guidelines for Americans has removed their previous dietary limits for cholesterol consumption due to a lack of supporting evidence (although they still suggest consuming as little cholesterol as possible) (1).

But, most people are still avoiding cholesterol-containing foods like eggs and red meat, and the incredibly harmful and dangerous cholesterol-lowering drugs are still the most prescribed drugs in the United States (2).

The anti-cholesterol story began with the notion that high blood cholesterol levels cause plaque formation, which causes heart attacks. This led to the recommendations to reduce dietary cholesterol, which are still pervasive today.

But, not only does cholesterol not cause plaque formation or heart attacks, it actually protects against them and is one of the most protective nutrients available to our bodies.

 

Cholesterol Does NOT Cause Heart Disease

Efforts to link cholesterol to heart disease have gone on for half a century and have failed miserably.

Well, I guess it depends how you define “failed,” considering the amount of cholesterol-lowering drugs sold and the persistence of the anti-cholesterol dietary advice. But as far as scientific evidence goes, they have certainly failed.

The most influential heart disease study ever done found that the cholesterol levels between those who developed heart disease and those who didn’t were nearly identical (3).

This hardly supports that cholesterol causes heart disease, and many other studies have found that people with higher levels of cholesterol are less likely to die from heart disease and that those with heart disease who have higher cholesterol levels are less likely to die from any cause (4, 5, 6, 7, 8).

This is not to mention that the amount of cholesterol we eat doesn’t affect our blood levels of cholesterol or our risk of heart disease! (9, 10) Our bodies produce their own cholesterol, so the amount of cholesterol we consume has little effect on the amount of cholesterol in our bodies.

In fact, our bodies use between 1,000 and 2,000 mg of cholesterol per day, and if we reduce the amount of cholesterol we consume then our bodies simply make more in response.

So, not only do the cholesterol levels in our blood not cause heart disease, eating high-cholesterol foods doesn’t increase those levels anyway!

But what about the plaques that form in our arteries and cause heart attacks? Aren’t they made up of cholesterol?

Yeah, partially. But, blaming cholesterol for the plaque is kind of like blaming firemen for a fire.

As you’ll read about in a little bit, cholesterol is a vital part of our immune system. So, while it is found in atherosclerotic plaques, it’s there as a protective factor rather than a cause (11). Polyunsaturated fats (PUFA) and their metabolites, on the other hand, are also found in these plaques and play a more causative role by contributing to oxidation and inflammation (12, 13, 14, 15).

But, while cholesterol levels, plaque, and heart disease aren’t affected by the amount of cholesterol we eat, they are directly affected by our metabolism.

 

Cholesterol and Metabolism

Cholesterol levels are influenced by many different variables, but the factor that has the largest effect is metabolism. This relationship between cholesterol and metabolism has been known for 100 years but is now largely ignored (16, 17, 18).

When our metabolism is high, we produce more cholesterol. But, we also use more cholesterol to produce the protective steroid hormones (and for other uses), which reduces the amount of cholesterol in our blood (18).

The opposite occurs when our metabolism is low. We produce less cholesterol and use less of it to produce the protective hormones, leaving more of it in the blood (18).

So, while the larger amount of cholesterol in the blood isn’t a problem on its own, it’s representative of a low metabolism, which is a problem and is associated with heart disease (19, 20). Plus, it means the body is using less cholesterol, which is also a problem due to cholesterol’s beneficial effects.

 

The Protective Effects of Cholesterol

Cholesterol is one of the most protective nutrients that exist in our bodies. It’s vital for brain function, immune function, and digestion, and is the precursor to the extremely important steroid hormones.

Our brains contain around 25% of all the cholesterol in our bodies because of its importance in brain function (21). And, a lack of cholesterol is associated with impaired cognitive function as well as depression and impaired mental health (22, 23).

Cholesterol also plays a major role in our immune system and is able to prevent infections and detoxify harmful toxins like endotoxin (11, 24, 25).

And, due to cholesterol’s protective effects, low cholesterol and cholesterol-lowering drugs have been shown to increase the risk of cancer and all-cause mortality (26, 27).

In other words, we can stop with the anti-cholesterol nonsense!

We NEED cholesterol and we don’t need to avoid foods that contain it (like eggs and other animal foods) or that increase our bodies production of it (like sugar and saturated fat). In fact, the cholesterol-producing and metabolism-supporting effects of these foods make them some of the best foods for supporting health.

If you have high cholesterol then a low metabolism is to blame, not these foods, and a cholesterol-lowering drug is not the answer.

 

References

The Cholesterol Nonsense Continues

I really thought we were done with all the anti-cholesterol nonsense, but it just won’t go away.

The anti-cholesterol narrative has been thoroughly discredited over the past couple decades, and even the Dietary Guidelines for Americans has removed their previous dietary limits for cholesterol consumption due to a lack of supporting evidence (although they still suggest consuming as little cholesterol as possible) (1).

But, most people are still avoiding cholesterol-containing foods like eggs and red meat, and the incredibly harmful and dangerous cholesterol-lowering drugs are still the most prescribed drugs in the United States (2).

The anti-cholesterol story began with the notion that high blood cholesterol levels cause plaque formation, which causes heart attacks. This led to the recommendations to reduce dietary cholesterol, which are still pervasive today.

But, not only does cholesterol not cause plaque formation or heart attacks, it actually protects against them and is one of the most protective nutrients available to our bodies.

 

Cholesterol Does NOT Cause Heart Disease

Efforts to link cholesterol to heart disease have gone on for half a century and have failed miserably.

Well, I guess it depends how you define “failed,” considering the amount of cholesterol-lowering drugs sold and the persistence of the anti-cholesterol dietary advice. But as far as scientific evidence goes, they have certainly failed.

The most influential heart disease study ever done found that the cholesterol levels between those who developed heart disease and those who didn’t were nearly identical (3).

This hardly supports that cholesterol causes heart disease, and many other studies have found that people with higher levels of cholesterol are less likely to die from heart disease and that those with heart disease who have higher cholesterol levels are less likely to die from any cause (4, 5, 6, 7, 8).

This is not to mention that the amount of cholesterol we eat doesn’t affect our blood levels of cholesterol or our risk of heart disease! (9, 10) Our bodies produce their own cholesterol, so the amount of cholesterol we consume has little effect on the amount of cholesterol in our bodies.

In fact, our bodies use between 1,000 and 2,000 mg of cholesterol per day, and if we reduce the amount of cholesterol we consume then our bodies simply make more in response.

So, not only do the cholesterol levels in our blood not cause heart disease, eating high-cholesterol foods doesn’t increase those levels anyway!

But what about the plaques that form in our arteries and cause heart attacks? Aren’t they made up of cholesterol?

Yeah, partially. But, blaming cholesterol for the plaque is kind of like blaming firemen for a fire.

As you’ll read about in a little bit, cholesterol is a vital part of our immune system. So, while it is found in atherosclerotic plaques, it’s there as a protective factor rather than a cause (11). Polyunsaturated fats (PUFA) and their metabolites, on the other hand, are also found in these plaques and play a more causative role by contributing to oxidation and inflammation (12, 13, 14, 15).

But, while cholesterol levels, plaque, and heart disease aren’t affected by the amount of cholesterol we eat, they are directly affected by our metabolism.

 

Cholesterol and Metabolism

Cholesterol levels are influenced by many different variables, but the factor that has the largest effect is metabolism. This relationship between cholesterol and metabolism has been known for 100 years but is now largely ignored (16, 17, 18).

When our metabolism is high, we produce more cholesterol. But, we also use more cholesterol to produce the protective steroid hormones (and for other uses), which reduces the amount of cholesterol in our blood (18).

The opposite occurs when our metabolism is low. We produce less cholesterol and use less of it to produce the protective hormones, leaving more of it in the blood (18).

So, while the larger amount of cholesterol in the blood isn’t a problem on its own, it’s representative of a low metabolism, which is a problem and is associated with heart disease (19, 20). Plus, it means the body is using less cholesterol, which is also a problem due to cholesterol’s beneficial effects.

 

The Protective Effects of Cholesterol

Cholesterol is one of the most protective nutrients that exist in our bodies. It’s vital for brain function, immune function, and digestion, and is the precursor to the extremely important steroid hormones.

Our brains contain around 25% of all the cholesterol in our bodies because of its importance in brain function (21). And, a lack of cholesterol is associated with impaired cognitive function as well as depression and impaired mental health (22, 23).

Cholesterol also plays a major role in our immune system and is able to prevent infections and detoxify harmful toxins like endotoxin (11, 24, 25).

And, due to cholesterol’s protective effects, low cholesterol and cholesterol-lowering drugs have been shown to increase the risk of cancer and all-cause mortality (26, 27).

In other words, we can stop with the anti-cholesterol nonsense!

We NEED cholesterol and we don’t need to avoid foods that contain it (like eggs and other animal foods) or that increase our bodies production of it (like sugar and saturated fat). In fact, the cholesterol-producing and metabolism-supporting effects of these foods make them some of the best foods for supporting health.

If you have high cholesterol then a low metabolism is to blame, not these foods, and a cholesterol-lowering drug is not the answer.

 

References

The Cholesterol Nonsense Continues

I really thought we were done with all the anti-cholesterol nonsense, but it just won’t go away.

The anti-cholesterol narrative has been thoroughly discredited over the past couple decades, and even the Dietary Guidelines for Americans has removed their previous dietary limits for cholesterol consumption due to a lack of supporting evidence (although they still suggest consuming as little cholesterol as possible) (1).

But, most people are still avoiding cholesterol-containing foods like eggs and red meat, and the incredibly harmful and dangerous cholesterol-lowering drugs are still the most prescribed drugs in the United States (2).

The anti-cholesterol story began with the notion that high blood cholesterol levels cause plaque formation, which causes heart attacks. This led to the recommendations to reduce dietary cholesterol, which are still pervasive today.

But, not only does cholesterol not cause plaque formation or heart attacks, it actually protects against them and is one of the most protective nutrients available to our bodies.

 

Cholesterol Does NOT Cause Heart Disease

Efforts to link cholesterol to heart disease have gone on for half a century and have failed miserably.

Well, I guess it depends how you define “failed,” considering the amount of cholesterol-lowering drugs sold and the persistence of the anti-cholesterol dietary advice. But as far as scientific evidence goes, they have certainly failed.

The most influential heart disease study ever done found that the cholesterol levels between those who developed heart disease and those who didn’t were nearly identical (3).

This hardly supports that cholesterol causes heart disease, and many other studies have found that people with higher levels of cholesterol are less likely to die from heart disease and that those with heart disease who have higher cholesterol levels are less likely to die from any cause (4, 5, 6, 7, 8).

This is not to mention that the amount of cholesterol we eat doesn’t affect our blood levels of cholesterol or our risk of heart disease! (9, 10) Our bodies produce their own cholesterol, so the amount of cholesterol we consume has little effect on the amount of cholesterol in our bodies.

In fact, our bodies use between 1,000 and 2,000 mg of cholesterol per day, and if we reduce the amount of cholesterol we consume then our bodies simply make more in response.

So, not only do the cholesterol levels in our blood not cause heart disease, eating high-cholesterol foods doesn’t increase those levels anyway!

But what about the plaques that form in our arteries and cause heart attacks? Aren’t they made up of cholesterol?

Yeah, partially. But, blaming cholesterol for the plaque is kind of like blaming firemen for a fire.

As you’ll read about in a little bit, cholesterol is a vital part of our immune system. So, while it is found in atherosclerotic plaques, it’s there as a protective factor rather than a cause (11). Polyunsaturated fats (PUFA) and their metabolites, on the other hand, are also found in these plaques and play a more causative role by contributing to oxidation and inflammation (12, 13, 14, 15).

But, while cholesterol levels, plaque, and heart disease aren’t affected by the amount of cholesterol we eat, they are directly affected by our metabolism.

 

Cholesterol and Metabolism

Cholesterol levels are influenced by many different variables, but the factor that has the largest effect is metabolism. This relationship between cholesterol and metabolism has been known for 100 years but is now largely ignored (16, 17, 18).

When our metabolism is high, we produce more cholesterol. But, we also use more cholesterol to produce the protective steroid hormones (and for other uses), which reduces the amount of cholesterol in our blood (18).

The opposite occurs when our metabolism is low. We produce less cholesterol and use less of it to produce the protective hormones, leaving more of it in the blood (18).

So, while the larger amount of cholesterol in the blood isn’t a problem on its own, it’s representative of a low metabolism, which is a problem and is associated with heart disease (19, 20). Plus, it means the body is using less cholesterol, which is also a problem due to cholesterol’s beneficial effects.

 

The Protective Effects of Cholesterol

Cholesterol is one of the most protective nutrients that exist in our bodies. It’s vital for brain function, immune function, and digestion, and is the precursor to the extremely important steroid hormones.

Our brains contain around 25% of all the cholesterol in our bodies because of its importance in brain function (21). And, a lack of cholesterol is associated with impaired cognitive function as well as depression and impaired mental health (22, 23).

Cholesterol also plays a major role in our immune system and is able to prevent infections and detoxify harmful toxins like endotoxin (11, 24, 25).

And, due to cholesterol’s protective effects, low cholesterol and cholesterol-lowering drugs have been shown to increase the risk of cancer and all-cause mortality (26, 27).

In other words, we can stop with the anti-cholesterol nonsense!

We NEED cholesterol and we don’t need to avoid foods that contain it (like eggs and other animal foods) or that increase our bodies production of it (like sugar and saturated fat). In fact, the cholesterol-producing and metabolism-supporting effects of these foods make them some of the best foods for supporting health.

If you have high cholesterol then a low metabolism is to blame, not these foods, and a cholesterol-lowering drug is not the answer.

 

References

The Cholesterol Nonsense Continues

I really thought we were done with all the anti-cholesterol nonsense, but it just won’t go away.

The anti-cholesterol narrative has been thoroughly discredited over the past couple decades, and even the Dietary Guidelines for Americans has removed their previous dietary limits for cholesterol consumption due to a lack of supporting evidence (although they still suggest consuming as little cholesterol as possible) (1).

But, most people are still avoiding cholesterol-containing foods like eggs and red meat, and the incredibly harmful and dangerous cholesterol-lowering drugs are still the most prescribed drugs in the United States (2).

The anti-cholesterol story began with the notion that high blood cholesterol levels cause plaque formation, which causes heart attacks. This led to the recommendations to reduce dietary cholesterol, which are still pervasive today.

But, not only does cholesterol not cause plaque formation or heart attacks, it actually protects against them and is one of the most protective nutrients available to our bodies.

 

Cholesterol Does NOT Cause Heart Disease

Efforts to link cholesterol to heart disease have gone on for half a century and have failed miserably.

Well, I guess it depends how you define “failed,” considering the amount of cholesterol-lowering drugs sold and the persistence of the anti-cholesterol dietary advice. But as far as scientific evidence goes, they have certainly failed.

The most influential heart disease study ever done found that the cholesterol levels between those who developed heart disease and those who didn’t were nearly identical (3).

This hardly supports that cholesterol causes heart disease, and many other studies have found that people with higher levels of cholesterol are less likely to die from heart disease and that those with heart disease who have higher cholesterol levels are less likely to die from any cause (4, 5, 6, 7, 8).

This is not to mention that the amount of cholesterol we eat doesn’t affect our blood levels of cholesterol or our risk of heart disease! (9, 10) Our bodies produce their own cholesterol, so the amount of cholesterol we consume has little effect on the amount of cholesterol in our bodies.

In fact, our bodies use between 1,000 and 2,000 mg of cholesterol per day, and if we reduce the amount of cholesterol we consume then our bodies simply make more in response.

So, not only do the cholesterol levels in our blood not cause heart disease, eating high-cholesterol foods doesn’t increase those levels anyway!

But what about the plaques that form in our arteries and cause heart attacks? Aren’t they made up of cholesterol?

Yeah, partially. But, blaming cholesterol for the plaque is kind of like blaming firemen for a fire.

As you’ll read about in a little bit, cholesterol is a vital part of our immune system. So, while it is found in atherosclerotic plaques, it’s there as a protective factor rather than a cause (11). Polyunsaturated fats (PUFA) and their metabolites, on the other hand, are also found in these plaques and play a more causative role by contributing to oxidation and inflammation (12, 13, 14, 15).

But, while cholesterol levels, plaque, and heart disease aren’t affected by the amount of cholesterol we eat, they are directly affected by our metabolism.

 

Cholesterol and Metabolism

Cholesterol levels are influenced by many different variables, but the factor that has the largest effect is metabolism. This relationship between cholesterol and metabolism has been known for 100 years but is now largely ignored (16, 17, 18).

When our metabolism is high, we produce more cholesterol. But, we also use more cholesterol to produce the protective steroid hormones (and for other uses), which reduces the amount of cholesterol in our blood (18).

The opposite occurs when our metabolism is low. We produce less cholesterol and use less of it to produce the protective hormones, leaving more of it in the blood (18).

So, while the larger amount of cholesterol in the blood isn’t a problem on its own, it’s representative of a low metabolism, which is a problem and is associated with heart disease (19, 20). Plus, it means the body is using less cholesterol, which is also a problem due to cholesterol’s beneficial effects.

 

The Protective Effects of Cholesterol

Cholesterol is one of the most protective nutrients that exist in our bodies. It’s vital for brain function, immune function, and digestion, and is the precursor to the extremely important steroid hormones.

Our brains contain around 25% of all the cholesterol in our bodies because of its importance in brain function (21). And, a lack of cholesterol is associated with impaired cognitive function as well as depression and impaired mental health (22, 23).

Cholesterol also plays a major role in our immune system and is able to prevent infections and detoxify harmful toxins like endotoxin (11, 24, 25).

And, due to cholesterol’s protective effects, low cholesterol and cholesterol-lowering drugs have been shown to increase the risk of cancer and all-cause mortality (26, 27).

In other words, we can stop with the anti-cholesterol nonsense!

We NEED cholesterol and we don’t need to avoid foods that contain it (like eggs and other animal foods) or that increase our bodies production of it (like sugar and saturated fat). In fact, the cholesterol-producing and metabolism-supporting effects of these foods make them some of the best foods for supporting health.

If you have high cholesterol then a low metabolism is to blame, not these foods, and a cholesterol-lowering drug is not the answer.

 

References

The Cholesterol Nonsense Continues

I really thought we were done with all the anti-cholesterol nonsense, but it just won’t go away.

The anti-cholesterol narrative has been thoroughly discredited over the past couple decades, and even the Dietary Guidelines for Americans has removed their previous dietary limits for cholesterol consumption due to a lack of supporting evidence (although they still suggest consuming as little cholesterol as possible) (1).

But, most people are still avoiding cholesterol-containing foods like eggs and red meat, and the incredibly harmful and dangerous cholesterol-lowering drugs are still the most prescribed drugs in the United States (2).

The anti-cholesterol story began with the notion that high blood cholesterol levels cause plaque formation, which causes heart attacks. This led to the recommendations to reduce dietary cholesterol, which are still pervasive today.

But, not only does cholesterol not cause plaque formation or heart attacks, it actually protects against them and is one of the most protective nutrients available to our bodies.

 

Cholesterol Does NOT Cause Heart Disease

Efforts to link cholesterol to heart disease have gone on for half a century and have failed miserably.

Well, I guess it depends how you define “failed,” considering the amount of cholesterol-lowering drugs sold and the persistence of the anti-cholesterol dietary advice. But as far as scientific evidence goes, they have certainly failed.

The most influential heart disease study ever done found that the cholesterol levels between those who developed heart disease and those who didn’t were nearly identical (3).

This hardly supports that cholesterol causes heart disease, and many other studies have found that people with higher levels of cholesterol are less likely to die from heart disease and that those with heart disease who have higher cholesterol levels are less likely to die from any cause (4, 5, 6, 7, 8).

This is not to mention that the amount of cholesterol we eat doesn’t affect our blood levels of cholesterol or our risk of heart disease! (9, 10) Our bodies produce their own cholesterol, so the amount of cholesterol we consume has little effect on the amount of cholesterol in our bodies.

In fact, our bodies use between 1,000 and 2,000 mg of cholesterol per day, and if we reduce the amount of cholesterol we consume then our bodies simply make more in response.

So, not only do the cholesterol levels in our blood not cause heart disease, eating high-cholesterol foods doesn’t increase those levels anyway!

But what about the plaques that form in our arteries and cause heart attacks? Aren’t they made up of cholesterol?

Yeah, partially. But, blaming cholesterol for the plaque is kind of like blaming firemen for a fire.

As you’ll read about in a little bit, cholesterol is a vital part of our immune system. So, while it is found in atherosclerotic plaques, it’s there as a protective factor rather than a cause (11). Polyunsaturated fats (PUFA) and their metabolites, on the other hand, are also found in these plaques and play a more causative role by contributing to oxidation and inflammation (12, 13, 14, 15).

But, while cholesterol levels, plaque, and heart disease aren’t affected by the amount of cholesterol we eat, they are directly affected by our metabolism.

 

Cholesterol and Metabolism

Cholesterol levels are influenced by many different variables, but the factor that has the largest effect is metabolism. This relationship between cholesterol and metabolism has been known for 100 years but is now largely ignored (16, 17, 18).

When our metabolism is high, we produce more cholesterol. But, we also use more cholesterol to produce the protective steroid hormones (and for other uses), which reduces the amount of cholesterol in our blood (18).

The opposite occurs when our metabolism is low. We produce less cholesterol and use less of it to produce the protective hormones, leaving more of it in the blood (18).

So, while the larger amount of cholesterol in the blood isn’t a problem on its own, it’s representative of a low metabolism, which is a problem and is associated with heart disease (19, 20). Plus, it means the body is using less cholesterol, which is also a problem due to cholesterol’s beneficial effects.

 

The Protective Effects of Cholesterol

Cholesterol is one of the most protective nutrients that exist in our bodies. It’s vital for brain function, immune function, and digestion, and is the precursor to the extremely important steroid hormones.

Our brains contain around 25% of all the cholesterol in our bodies because of its importance in brain function (21). And, a lack of cholesterol is associated with impaired cognitive function as well as depression and impaired mental health (22, 23).

Cholesterol also plays a major role in our immune system and is able to prevent infections and detoxify harmful toxins like endotoxin (11, 24, 25).

And, due to cholesterol’s protective effects, low cholesterol and cholesterol-lowering drugs have been shown to increase the risk of cancer and all-cause mortality (26, 27).

In other words, we can stop with the anti-cholesterol nonsense!

We NEED cholesterol and we don’t need to avoid foods that contain it (like eggs and other animal foods) or that increase our bodies production of it (like sugar and saturated fat). In fact, the cholesterol-producing and metabolism-supporting effects of these foods make them some of the best foods for supporting health.

If you have high cholesterol then a low metabolism is to blame, not these foods, and a cholesterol-lowering drug is not the answer.

 

References

The Cholesterol Nonsense Continues

I really thought we were done with all the anti-cholesterol nonsense, but it just won’t go away.

The anti-cholesterol narrative has been thoroughly discredited over the past couple decades, and even the Dietary Guidelines for Americans has removed their previous dietary limits for cholesterol consumption due to a lack of supporting evidence (although they still suggest consuming as little cholesterol as possible) (1).

But, most people are still avoiding cholesterol-containing foods like eggs and red meat, and the incredibly harmful and dangerous cholesterol-lowering drugs are still the most prescribed drugs in the United States (2).

The anti-cholesterol story began with the notion that high blood cholesterol levels cause plaque formation, which causes heart attacks. This led to the recommendations to reduce dietary cholesterol, which are still pervasive today.

But, not only does cholesterol not cause plaque formation or heart attacks, it actually protects against them and is one of the most protective nutrients available to our bodies.

 

Cholesterol Does NOT Cause Heart Disease

Efforts to link cholesterol to heart disease have gone on for half a century and have failed miserably.

Well, I guess it depends how you define “failed,” considering the amount of cholesterol-lowering drugs sold and the persistence of the anti-cholesterol dietary advice. But as far as scientific evidence goes, they have certainly failed.

The most influential heart disease study ever done found that the cholesterol levels between those who developed heart disease and those who didn’t were nearly identical (3).

This hardly supports that cholesterol causes heart disease, and many other studies have found that people with higher levels of cholesterol are less likely to die from heart disease and that those with heart disease who have higher cholesterol levels are less likely to die from any cause (4, 5, 6, 7, 8).

This is not to mention that the amount of cholesterol we eat doesn’t affect our blood levels of cholesterol or our risk of heart disease! (9, 10) Our bodies produce their own cholesterol, so the amount of cholesterol we consume has little effect on the amount of cholesterol in our bodies.

In fact, our bodies use between 1,000 and 2,000 mg of cholesterol per day, and if we reduce the amount of cholesterol we consume then our bodies simply make more in response.

So, not only do the cholesterol levels in our blood not cause heart disease, eating high-cholesterol foods doesn’t increase those levels anyway!

But what about the plaques that form in our arteries and cause heart attacks? Aren’t they made up of cholesterol?

Yeah, partially. But, blaming cholesterol for the plaque is kind of like blaming firemen for a fire.

As you’ll read about in a little bit, cholesterol is a vital part of our immune system. So, while it is found in atherosclerotic plaques, it’s there as a protective factor rather than a cause (11). Polyunsaturated fats (PUFA) and their metabolites, on the other hand, are also found in these plaques and play a more causative role by contributing to oxidation and inflammation (12, 13, 14, 15).

But, while cholesterol levels, plaque, and heart disease aren’t affected by the amount of cholesterol we eat, they are directly affected by our metabolism.

 

Cholesterol and Metabolism

Cholesterol levels are influenced by many different variables, but the factor that has the largest effect is metabolism. This relationship between cholesterol and metabolism has been known for 100 years but is now largely ignored (16, 17, 18).

When our metabolism is high, we produce more cholesterol. But, we also use more cholesterol to produce the protective steroid hormones (and for other uses), which reduces the amount of cholesterol in our blood (18).

The opposite occurs when our metabolism is low. We produce less cholesterol and use less of it to produce the protective hormones, leaving more of it in the blood (18).

So, while the larger amount of cholesterol in the blood isn’t a problem on its own, it’s representative of a low metabolism, which is a problem and is associated with heart disease (19, 20). Plus, it means the body is using less cholesterol, which is also a problem due to cholesterol’s beneficial effects.

 

The Protective Effects of Cholesterol

Cholesterol is one of the most protective nutrients that exist in our bodies. It’s vital for brain function, immune function, and digestion, and is the precursor to the extremely important steroid hormones.

Our brains contain around 25% of all the cholesterol in our bodies because of its importance in brain function (21). And, a lack of cholesterol is associated with impaired cognitive function as well as depression and impaired mental health (22, 23).

Cholesterol also plays a major role in our immune system and is able to prevent infections and detoxify harmful toxins like endotoxin (11, 24, 25).

And, due to cholesterol’s protective effects, low cholesterol and cholesterol-lowering drugs have been shown to increase the risk of cancer and all-cause mortality (26, 27).

In other words, we can stop with the anti-cholesterol nonsense!

We NEED cholesterol and we don’t need to avoid foods that contain it (like eggs and other animal foods) or that increase our bodies production of it (like sugar and saturated fat). In fact, the cholesterol-producing and metabolism-supporting effects of these foods make them some of the best foods for supporting health.

If you have high cholesterol then a low metabolism is to blame, not these foods, and a cholesterol-lowering drug is not the answer.

 

References

The Cholesterol Nonsense Continues

I really thought we were done with all the anti-cholesterol nonsense, but it just won’t go away.

The anti-cholesterol narrative has been thoroughly discredited over the past couple decades, and even the Dietary Guidelines for Americans has removed their previous dietary limits for cholesterol consumption due to a lack of supporting evidence (although they still suggest consuming as little cholesterol as possible) (1).

But, most people are still avoiding cholesterol-containing foods like eggs and red meat, and the incredibly harmful and dangerous cholesterol-lowering drugs are still the most prescribed drugs in the United States (2).

The anti-cholesterol story began with the notion that high blood cholesterol levels cause plaque formation, which causes heart attacks. This led to the recommendations to reduce dietary cholesterol, which are still pervasive today.

But, not only does cholesterol not cause plaque formation or heart attacks, it actually protects against them and is one of the most protective nutrients available to our bodies.

 

Cholesterol Does NOT Cause Heart Disease

Efforts to link cholesterol to heart disease have gone on for half a century and have failed miserably.

Well, I guess it depends how you define “failed,” considering the amount of cholesterol-lowering drugs sold and the persistence of the anti-cholesterol dietary advice. But as far as scientific evidence goes, they have certainly failed.

The most influential heart disease study ever done found that the cholesterol levels between those who developed heart disease and those who didn’t were nearly identical (3).

This hardly supports that cholesterol causes heart disease, and many other studies have found that people with higher levels of cholesterol are less likely to die from heart disease and that those with heart disease who have higher cholesterol levels are less likely to die from any cause (4, 5, 6, 7, 8).

This is not to mention that the amount of cholesterol we eat doesn’t affect our blood levels of cholesterol or our risk of heart disease! (9, 10) Our bodies produce their own cholesterol, so the amount of cholesterol we consume has little effect on the amount of cholesterol in our bodies.

In fact, our bodies use between 1,000 and 2,000 mg of cholesterol per day, and if we reduce the amount of cholesterol we consume then our bodies simply make more in response.

So, not only do the cholesterol levels in our blood not cause heart disease, eating high-cholesterol foods doesn’t increase those levels anyway!

But what about the plaques that form in our arteries and cause heart attacks? Aren’t they made up of cholesterol?

Yeah, partially. But, blaming cholesterol for the plaque is kind of like blaming firemen for a fire.

As you’ll read about in a little bit, cholesterol is a vital part of our immune system. So, while it is found in atherosclerotic plaques, it’s there as a protective factor rather than a cause (11). Polyunsaturated fats (PUFA) and their metabolites, on the other hand, are also found in these plaques and play a more causative role by contributing to oxidation and inflammation (12, 13, 14, 15).

But, while cholesterol levels, plaque, and heart disease aren’t affected by the amount of cholesterol we eat, they are directly affected by our metabolism.

 

Cholesterol and Metabolism

Cholesterol levels are influenced by many different variables, but the factor that has the largest effect is metabolism. This relationship between cholesterol and metabolism has been known for 100 years but is now largely ignored (16, 17, 18).

When our metabolism is high, we produce more cholesterol. But, we also use more cholesterol to produce the protective steroid hormones (and for other uses), which reduces the amount of cholesterol in our blood (18).

The opposite occurs when our metabolism is low. We produce less cholesterol and use less of it to produce the protective hormones, leaving more of it in the blood (18).

So, while the larger amount of cholesterol in the blood isn’t a problem on its own, it’s representative of a low metabolism, which is a problem and is associated with heart disease (19, 20). Plus, it means the body is using less cholesterol, which is also a problem due to cholesterol’s beneficial effects.

 

The Protective Effects of Cholesterol

Cholesterol is one of the most protective nutrients that exist in our bodies. It’s vital for brain function, immune function, and digestion, and is the precursor to the extremely important steroid hormones.

Our brains contain around 25% of all the cholesterol in our bodies because of its importance in brain function (21). And, a lack of cholesterol is associated with impaired cognitive function as well as depression and impaired mental health (22, 23).

Cholesterol also plays a major role in our immune system and is able to prevent infections and detoxify harmful toxins like endotoxin (11, 24, 25).

And, due to cholesterol’s protective effects, low cholesterol and cholesterol-lowering drugs have been shown to increase the risk of cancer and all-cause mortality (26, 27).

In other words, we can stop with the anti-cholesterol nonsense!

We NEED cholesterol and we don’t need to avoid foods that contain it (like eggs and other animal foods) or that increase our bodies production of it (like sugar and saturated fat). In fact, the cholesterol-producing and metabolism-supporting effects of these foods make them some of the best foods for supporting health.

If you have high cholesterol then a low metabolism is to blame, not these foods, and a cholesterol-lowering drug is not the answer.

 

References

The Cholesterol Nonsense Continues

I really thought we were done with all the anti-cholesterol nonsense, but it just won’t go away.

The anti-cholesterol narrative has been thoroughly discredited over the past couple decades, and even the Dietary Guidelines for Americans has removed their previous dietary limits for cholesterol consumption due to a lack of supporting evidence (although they still suggest consuming as little cholesterol as possible) (1).

But, most people are still avoiding cholesterol-containing foods like eggs and red meat, and the incredibly harmful and dangerous cholesterol-lowering drugs are still the most prescribed drugs in the United States (2).

The anti-cholesterol story began with the notion that high blood cholesterol levels cause plaque formation, which causes heart attacks. This led to the recommendations to reduce dietary cholesterol, which are still pervasive today.

But, not only does cholesterol not cause plaque formation or heart attacks, it actually protects against them and is one of the most protective nutrients available to our bodies.

 

Cholesterol Does NOT Cause Heart Disease

Efforts to link cholesterol to heart disease have gone on for half a century and have failed miserably.

Well, I guess it depends how you define “failed,” considering the amount of cholesterol-lowering drugs sold and the persistence of the anti-cholesterol dietary advice. But as far as scientific evidence goes, they have certainly failed.

The most influential heart disease study ever done found that the cholesterol levels between those who developed heart disease and those who didn’t were nearly identical (3).

This hardly supports that cholesterol causes heart disease, and many other studies have found that people with higher levels of cholesterol are less likely to die from heart disease and that those with heart disease who have higher cholesterol levels are less likely to die from any cause (4, 5, 6, 7, 8).

This is not to mention that the amount of cholesterol we eat doesn’t affect our blood levels of cholesterol or our risk of heart disease! (9, 10) Our bodies produce their own cholesterol, so the amount of cholesterol we consume has little effect on the amount of cholesterol in our bodies.

In fact, our bodies use between 1,000 and 2,000 mg of cholesterol per day, and if we reduce the amount of cholesterol we consume then our bodies simply make more in response.

So, not only do the cholesterol levels in our blood not cause heart disease, eating high-cholesterol foods doesn’t increase those levels anyway!

But what about the plaques that form in our arteries and cause heart attacks? Aren’t they made up of cholesterol?

Yeah, partially. But, blaming cholesterol for the plaque is kind of like blaming firemen for a fire.

As you’ll read about in a little bit, cholesterol is a vital part of our immune system. So, while it is found in atherosclerotic plaques, it’s there as a protective factor rather than a cause (11). Polyunsaturated fats (PUFA) and their metabolites, on the other hand, are also found in these plaques and play a more causative role by contributing to oxidation and inflammation (12, 13, 14, 15).

But, while cholesterol levels, plaque, and heart disease aren’t affected by the amount of cholesterol we eat, they are directly affected by our metabolism.

 

Cholesterol and Metabolism

Cholesterol levels are influenced by many different variables, but the factor that has the largest effect is metabolism. This relationship between cholesterol and metabolism has been known for 100 years but is now largely ignored (16, 17, 18).

When our metabolism is high, we produce more cholesterol. But, we also use more cholesterol to produce the protective steroid hormones (and for other uses), which reduces the amount of cholesterol in our blood (18).

The opposite occurs when our metabolism is low. We produce less cholesterol and use less of it to produce the protective hormones, leaving more of it in the blood (18).

So, while the larger amount of cholesterol in the blood isn’t a problem on its own, it’s representative of a low metabolism, which is a problem and is associated with heart disease (19, 20). Plus, it means the body is using less cholesterol, which is also a problem due to cholesterol’s beneficial effects.

 

The Protective Effects of Cholesterol

Cholesterol is one of the most protective nutrients that exist in our bodies. It’s vital for brain function, immune function, and digestion, and is the precursor to the extremely important steroid hormones.

Our brains contain around 25% of all the cholesterol in our bodies because of its importance in brain function (21). And, a lack of cholesterol is associated with impaired cognitive function as well as depression and impaired mental health (22, 23).

Cholesterol also plays a major role in our immune system and is able to prevent infections and detoxify harmful toxins like endotoxin (11, 24, 25).

And, due to cholesterol’s protective effects, low cholesterol and cholesterol-lowering drugs have been shown to increase the risk of cancer and all-cause mortality (26, 27).

In other words, we can stop with the anti-cholesterol nonsense!

We NEED cholesterol and we don’t need to avoid foods that contain it (like eggs and other animal foods) or that increase our bodies production of it (like sugar and saturated fat). In fact, the cholesterol-producing and metabolism-supporting effects of these foods make them some of the best foods for supporting health.

If you have high cholesterol then a low metabolism is to blame, not these foods, and a cholesterol-lowering drug is not the answer.

 

References

The Cholesterol Nonsense Continues

I really thought we were done with all the anti-cholesterol nonsense, but it just won’t go away.

The anti-cholesterol narrative has been thoroughly discredited over the past couple decades, and even the Dietary Guidelines for Americans has removed their previous dietary limits for cholesterol consumption due to a lack of supporting evidence (although they still suggest consuming as little cholesterol as possible) (1).

But, most people are still avoiding cholesterol-containing foods like eggs and red meat, and the incredibly harmful and dangerous cholesterol-lowering drugs are still the most prescribed drugs in the United States (2).

The anti-cholesterol story began with the notion that high blood cholesterol levels cause plaque formation, which causes heart attacks. This led to the recommendations to reduce dietary cholesterol, which are still pervasive today.

But, not only does cholesterol not cause plaque formation or heart attacks, it actually protects against them and is one of the most protective nutrients available to our bodies.

 

Cholesterol Does NOT Cause Heart Disease

Efforts to link cholesterol to heart disease have gone on for half a century and have failed miserably.

Well, I guess it depends how you define “failed,” considering the amount of cholesterol-lowering drugs sold and the persistence of the anti-cholesterol dietary advice. But as far as scientific evidence goes, they have certainly failed.

The most influential heart disease study ever done found that the cholesterol levels between those who developed heart disease and those who didn’t were nearly identical (3).

This hardly supports that cholesterol causes heart disease, and many other studies have found that people with higher levels of cholesterol are less likely to die from heart disease and that those with heart disease who have higher cholesterol levels are less likely to die from any cause (4, 5, 6, 7, 8).

This is not to mention that the amount of cholesterol we eat doesn’t affect our blood levels of cholesterol or our risk of heart disease! (9, 10) Our bodies produce their own cholesterol, so the amount of cholesterol we consume has little effect on the amount of cholesterol in our bodies.

In fact, our bodies use between 1,000 and 2,000 mg of cholesterol per day, and if we reduce the amount of cholesterol we consume then our bodies simply make more in response.

So, not only do the cholesterol levels in our blood not cause heart disease, eating high-cholesterol foods doesn’t increase those levels anyway!

But what about the plaques that form in our arteries and cause heart attacks? Aren’t they made up of cholesterol?

Yeah, partially. But, blaming cholesterol for the plaque is kind of like blaming firemen for a fire.

As you’ll read about in a little bit, cholesterol is a vital part of our immune system. So, while it is found in atherosclerotic plaques, it’s there as a protective factor rather than a cause (11). Polyunsaturated fats (PUFA) and their metabolites, on the other hand, are also found in these plaques and play a more causative role by contributing to oxidation and inflammation (12, 13, 14, 15).

But, while cholesterol levels, plaque, and heart disease aren’t affected by the amount of cholesterol we eat, they are directly affected by our metabolism.

 

Cholesterol and Metabolism

Cholesterol levels are influenced by many different variables, but the factor that has the largest effect is metabolism. This relationship between cholesterol and metabolism has been known for 100 years but is now largely ignored (16, 17, 18).

When our metabolism is high, we produce more cholesterol. But, we also use more cholesterol to produce the protective steroid hormones (and for other uses), which reduces the amount of cholesterol in our blood (18).

The opposite occurs when our metabolism is low. We produce less cholesterol and use less of it to produce the protective hormones, leaving more of it in the blood (18).

So, while the larger amount of cholesterol in the blood isn’t a problem on its own, it’s representative of a low metabolism, which is a problem and is associated with heart disease (19, 20). Plus, it means the body is using less cholesterol, which is also a problem due to cholesterol’s beneficial effects.

 

The Protective Effects of Cholesterol

Cholesterol is one of the most protective nutrients that exist in our bodies. It’s vital for brain function, immune function, and digestion, and is the precursor to the extremely important steroid hormones.

Our brains contain around 25% of all the cholesterol in our bodies because of its importance in brain function (21). And, a lack of cholesterol is associated with impaired cognitive function as well as depression and impaired mental health (22, 23).

Cholesterol also plays a major role in our immune system and is able to prevent infections and detoxify harmful toxins like endotoxin (11, 24, 25).

And, due to cholesterol’s protective effects, low cholesterol and cholesterol-lowering drugs have been shown to increase the risk of cancer and all-cause mortality (26, 27).

In other words, we can stop with the anti-cholesterol nonsense!

We NEED cholesterol and we don’t need to avoid foods that contain it (like eggs and other animal foods) or that increase our bodies production of it (like sugar and saturated fat). In fact, the cholesterol-producing and metabolism-supporting effects of these foods make them some of the best foods for supporting health.

If you have high cholesterol then a low metabolism is to blame, not these foods, and a cholesterol-lowering drug is not the answer.

 

References

The Cholesterol Nonsense Continues

I really thought we were done with all the anti-cholesterol nonsense, but it just won’t go away.

The anti-cholesterol narrative has been thoroughly discredited over the past couple decades, and even the Dietary Guidelines for Americans has removed their previous dietary limits for cholesterol consumption due to a lack of supporting evidence (although they still suggest consuming as little cholesterol as possible) (1).

But, most people are still avoiding cholesterol-containing foods like eggs and red meat, and the incredibly harmful and dangerous cholesterol-lowering drugs are still the most prescribed drugs in the United States (2).

The anti-cholesterol story began with the notion that high blood cholesterol levels cause plaque formation, which causes heart attacks. This led to the recommendations to reduce dietary cholesterol, which are still pervasive today.

But, not only does cholesterol not cause plaque formation or heart attacks, it actually protects against them and is one of the most protective nutrients available to our bodies.

 

Cholesterol Does NOT Cause Heart Disease

Efforts to link cholesterol to heart disease have gone on for half a century and have failed miserably.

Well, I guess it depends how you define “failed,” considering the amount of cholesterol-lowering drugs sold and the persistence of the anti-cholesterol dietary advice. But as far as scientific evidence goes, they have certainly failed.

The most influential heart disease study ever done found that the cholesterol levels between those who developed heart disease and those who didn’t were nearly identical (3).

This hardly supports that cholesterol causes heart disease, and many other studies have found that people with higher levels of cholesterol are less likely to die from heart disease and that those with heart disease who have higher cholesterol levels are less likely to die from any cause (4, 5, 6, 7, 8).

This is not to mention that the amount of cholesterol we eat doesn’t affect our blood levels of cholesterol or our risk of heart disease! (9, 10) Our bodies produce their own cholesterol, so the amount of cholesterol we consume has little effect on the amount of cholesterol in our bodies.

In fact, our bodies use between 1,000 and 2,000 mg of cholesterol per day, and if we reduce the amount of cholesterol we consume then our bodies simply make more in response.

So, not only do the cholesterol levels in our blood not cause heart disease, eating high-cholesterol foods doesn’t increase those levels anyway!

But what about the plaques that form in our arteries and cause heart attacks? Aren’t they made up of cholesterol?

Yeah, partially. But, blaming cholesterol for the plaque is kind of like blaming firemen for a fire.

As you’ll read about in a little bit, cholesterol is a vital part of our immune system. So, while it is found in atherosclerotic plaques, it’s there as a protective factor rather than a cause (11). Polyunsaturated fats (PUFA) and their metabolites, on the other hand, are also found in these plaques and play a more causative role by contributing to oxidation and inflammation (12, 13, 14, 15).

But, while cholesterol levels, plaque, and heart disease aren’t affected by the amount of cholesterol we eat, they are directly affected by our metabolism.

 

Cholesterol and Metabolism

Cholesterol levels are influenced by many different variables, but the factor that has the largest effect is metabolism. This relationship between cholesterol and metabolism has been known for 100 years but is now largely ignored (16, 17, 18).

When our metabolism is high, we produce more cholesterol. But, we also use more cholesterol to produce the protective steroid hormones (and for other uses), which reduces the amount of cholesterol in our blood (18).

The opposite occurs when our metabolism is low. We produce less cholesterol and use less of it to produce the protective hormones, leaving more of it in the blood (18).

So, while the larger amount of cholesterol in the blood isn’t a problem on its own, it’s representative of a low metabolism, which is a problem and is associated with heart disease (19, 20). Plus, it means the body is using less cholesterol, which is also a problem due to cholesterol’s beneficial effects.

 

The Protective Effects of Cholesterol

Cholesterol is one of the most protective nutrients that exist in our bodies. It’s vital for brain function, immune function, and digestion, and is the precursor to the extremely important steroid hormones.

Our brains contain around 25% of all the cholesterol in our bodies because of its importance in brain function (21). And, a lack of cholesterol is associated with impaired cognitive function as well as depression and impaired mental health (22, 23).

Cholesterol also plays a major role in our immune system and is able to prevent infections and detoxify harmful toxins like endotoxin (11, 24, 25).

And, due to cholesterol’s protective effects, low cholesterol and cholesterol-lowering drugs have been shown to increase the risk of cancer and all-cause mortality (26, 27).

In other words, we can stop with the anti-cholesterol nonsense!

We NEED cholesterol and we don’t need to avoid foods that contain it (like eggs and other animal foods) or that increase our bodies production of it (like sugar and saturated fat). In fact, the cholesterol-producing and metabolism-supporting effects of these foods make them some of the best foods for supporting health.

If you have high cholesterol then a low metabolism is to blame, not these foods, and a cholesterol-lowering drug is not the answer.

 

References

The Cholesterol Nonsense Continues

I really thought we were done with all the anti-cholesterol nonsense, but it just won’t go away.

The anti-cholesterol narrative has been thoroughly discredited over the past couple decades, and even the Dietary Guidelines for Americans has removed their previous dietary limits for cholesterol consumption due to a lack of supporting evidence (although they still suggest consuming as little cholesterol as possible) (1).

But, most people are still avoiding cholesterol-containing foods like eggs and red meat, and the incredibly harmful and dangerous cholesterol-lowering drugs are still the most prescribed drugs in the United States (2).

The anti-cholesterol story began with the notion that high blood cholesterol levels cause plaque formation, which causes heart attacks. This led to the recommendations to reduce dietary cholesterol, which are still pervasive today.

But, not only does cholesterol not cause plaque formation or heart attacks, it actually protects against them and is one of the most protective nutrients available to our bodies.

 

Cholesterol Does NOT Cause Heart Disease

Efforts to link cholesterol to heart disease have gone on for half a century and have failed miserably.

Well, I guess it depends how you define “failed,” considering the amount of cholesterol-lowering drugs sold and the persistence of the anti-cholesterol dietary advice. But as far as scientific evidence goes, they have certainly failed.

The most influential heart disease study ever done found that the cholesterol levels between those who developed heart disease and those who didn’t were nearly identical (3).

This hardly supports that cholesterol causes heart disease, and many other studies have found that people with higher levels of cholesterol are less likely to die from heart disease and that those with heart disease who have higher cholesterol levels are less likely to die from any cause (4, 5, 6, 7, 8).

This is not to mention that the amount of cholesterol we eat doesn’t affect our blood levels of cholesterol or our risk of heart disease! (9, 10) Our bodies produce their own cholesterol, so the amount of cholesterol we consume has little effect on the amount of cholesterol in our bodies.

In fact, our bodies use between 1,000 and 2,000 mg of cholesterol per day, and if we reduce the amount of cholesterol we consume then our bodies simply make more in response.

So, not only do the cholesterol levels in our blood not cause heart disease, eating high-cholesterol foods doesn’t increase those levels anyway!

But what about the plaques that form in our arteries and cause heart attacks? Aren’t they made up of cholesterol?

Yeah, partially. But, blaming cholesterol for the plaque is kind of like blaming firemen for a fire.

As you’ll read about in a little bit, cholesterol is a vital part of our immune system. So, while it is found in atherosclerotic plaques, it’s there as a protective factor rather than a cause (11). Polyunsaturated fats (PUFA) and their metabolites, on the other hand, are also found in these plaques and play a more causative role by contributing to oxidation and inflammation (12, 13, 14, 15).

But, while cholesterol levels, plaque, and heart disease aren’t affected by the amount of cholesterol we eat, they are directly affected by our metabolism.

 

Cholesterol and Metabolism

Cholesterol levels are influenced by many different variables, but the factor that has the largest effect is metabolism. This relationship between cholesterol and metabolism has been known for 100 years but is now largely ignored (16, 17, 18).

When our metabolism is high, we produce more cholesterol. But, we also use more cholesterol to produce the protective steroid hormones (and for other uses), which reduces the amount of cholesterol in our blood (18).

The opposite occurs when our metabolism is low. We produce less cholesterol and use less of it to produce the protective hormones, leaving more of it in the blood (18).

So, while the larger amount of cholesterol in the blood isn’t a problem on its own, it’s representative of a low metabolism, which is a problem and is associated with heart disease (19, 20). Plus, it means the body is using less cholesterol, which is also a problem due to cholesterol’s beneficial effects.

 

The Protective Effects of Cholesterol

Cholesterol is one of the most protective nutrients that exist in our bodies. It’s vital for brain function, immune function, and digestion, and is the precursor to the extremely important steroid hormones.

Our brains contain around 25% of all the cholesterol in our bodies because of its importance in brain function (21). And, a lack of cholesterol is associated with impaired cognitive function as well as depression and impaired mental health (22, 23).

Cholesterol also plays a major role in our immune system and is able to prevent infections and detoxify harmful toxins like endotoxin (11, 24, 25).

And, due to cholesterol’s protective effects, low cholesterol and cholesterol-lowering drugs have been shown to increase the risk of cancer and all-cause mortality (26, 27).

In other words, we can stop with the anti-cholesterol nonsense!

We NEED cholesterol and we don’t need to avoid foods that contain it (like eggs and other animal foods) or that increase our bodies production of it (like sugar and saturated fat). In fact, the cholesterol-producing and metabolism-supporting effects of these foods make them some of the best foods for supporting health.

If you have high cholesterol then a low metabolism is to blame, not these foods, and a cholesterol-lowering drug is not the answer.

 

References

The Cholesterol Nonsense Continues

I really thought we were done with all the anti-cholesterol nonsense, but it just won’t go away.

The anti-cholesterol narrative has been thoroughly discredited over the past couple decades, and even the Dietary Guidelines for Americans has removed their previous dietary limits for cholesterol consumption due to a lack of supporting evidence (although they still suggest consuming as little cholesterol as possible) (1).

But, most people are still avoiding cholesterol-containing foods like eggs and red meat, and the incredibly harmful and dangerous cholesterol-lowering drugs are still the most prescribed drugs in the United States (2).

The anti-cholesterol story began with the notion that high blood cholesterol levels cause plaque formation, which causes heart attacks. This led to the recommendations to reduce dietary cholesterol, which are still pervasive today.

But, not only does cholesterol not cause plaque formation or heart attacks, it actually protects against them and is one of the most protective nutrients available to our bodies.

 

Cholesterol Does NOT Cause Heart Disease

Efforts to link cholesterol to heart disease have gone on for half a century and have failed miserably.

Well, I guess it depends how you define “failed,” considering the amount of cholesterol-lowering drugs sold and the persistence of the anti-cholesterol dietary advice. But as far as scientific evidence goes, they have certainly failed.

The most influential heart disease study ever done found that the cholesterol levels between those who developed heart disease and those who didn’t were nearly identical (3).

This hardly supports that cholesterol causes heart disease, and many other studies have found that people with higher levels of cholesterol are less likely to die from heart disease and that those with heart disease who have higher cholesterol levels are less likely to die from any cause (4, 5, 6, 7, 8).

This is not to mention that the amount of cholesterol we eat doesn’t affect our blood levels of cholesterol or our risk of heart disease! (9, 10) Our bodies produce their own cholesterol, so the amount of cholesterol we consume has little effect on the amount of cholesterol in our bodies.

In fact, our bodies use between 1,000 and 2,000 mg of cholesterol per day, and if we reduce the amount of cholesterol we consume then our bodies simply make more in response.

So, not only do the cholesterol levels in our blood not cause heart disease, eating high-cholesterol foods doesn’t increase those levels anyway!

But what about the plaques that form in our arteries and cause heart attacks? Aren’t they made up of cholesterol?

Yeah, partially. But, blaming cholesterol for the plaque is kind of like blaming firemen for a fire.

As you’ll read about in a little bit, cholesterol is a vital part of our immune system. So, while it is found in atherosclerotic plaques, it’s there as a protective factor rather than a cause (11). Polyunsaturated fats (PUFA) and their metabolites, on the other hand, are also found in these plaques and play a more causative role by contributing to oxidation and inflammation (12, 13, 14, 15).

But, while cholesterol levels, plaque, and heart disease aren’t affected by the amount of cholesterol we eat, they are directly affected by our metabolism.

 

Cholesterol and Metabolism

Cholesterol levels are influenced by many different variables, but the factor that has the largest effect is metabolism. This relationship between cholesterol and metabolism has been known for 100 years but is now largely ignored (16, 17, 18).

When our metabolism is high, we produce more cholesterol. But, we also use more cholesterol to produce the protective steroid hormones (and for other uses), which reduces the amount of cholesterol in our blood (18).

The opposite occurs when our metabolism is low. We produce less cholesterol and use less of it to produce the protective hormones, leaving more of it in the blood (18).

So, while the larger amount of cholesterol in the blood isn’t a problem on its own, it’s representative of a low metabolism, which is a problem and is associated with heart disease (19, 20). Plus, it means the body is using less cholesterol, which is also a problem due to cholesterol’s beneficial effects.

 

The Protective Effects of Cholesterol

Cholesterol is one of the most protective nutrients that exist in our bodies. It’s vital for brain function, immune function, and digestion, and is the precursor to the extremely important steroid hormones.

Our brains contain around 25% of all the cholesterol in our bodies because of its importance in brain function (21). And, a lack of cholesterol is associated with impaired cognitive function as well as depression and impaired mental health (22, 23).

Cholesterol also plays a major role in our immune system and is able to prevent infections and detoxify harmful toxins like endotoxin (11, 24, 25).

And, due to cholesterol’s protective effects, low cholesterol and cholesterol-lowering drugs have been shown to increase the risk of cancer and all-cause mortality (26, 27).

In other words, we can stop with the anti-cholesterol nonsense!

We NEED cholesterol and we don’t need to avoid foods that contain it (like eggs and other animal foods) or that increase our bodies production of it (like sugar and saturated fat). In fact, the cholesterol-producing and metabolism-supporting effects of these foods make them some of the best foods for supporting health.

If you have high cholesterol then a low metabolism is to blame, not these foods, and a cholesterol-lowering drug is not the answer.

 

References

Sugar Does NOT Cause Inflammation (Part 2)

In part 1 of this series, I explained some of the basic physiology underlying what happens when we consume sugar. I also explained why, while sugar can cause inflammation, it takes A LOT of sugar and the inflammation it causes isn’t necessarily harmful.

In this article, I’m going to explore this topic a little more in depth and explain why the research behind sugar causing inflammation is so misleading.

But before we dive into the research I’d like to first mention that I’m not going to include observational studies (association-based population studies).

There are many confounding variables in these types of studies, the biggest one being that sugar is widely considered unhealthy. So, those that consume more sugar typically care less about their health and do other unhealthy things. And the opposite is true for those who consume less sugar. (How many people do you know who try to be healthy but also drink soda every day and have doughnuts for breakfast?)

Those studies aside, there are many research studies that conclude that sugar, specifically fructose, causes inflammation. So, let’s start there.

 

Research Shows That Sugar Causes Inflammation

In chronic conditions like diabetes, heart disease, cancer, autoimmune conditions, and obesity, several markers are elevated that indicate chronic inflammation: triglycerides, free fatty acids, fasting blood glucose, fasting insulin, blood pressure, cholesterol, LDL, VLDL, TNF-a, NF-kb, IL-6, etc.

These markers are all symptoms of an inability to produce energy, which ends up causing the perpetual damage that we associate with these conditions.

For many decades, saturated fat was blamed for causing these conditions and was shown to increase these markers. But after saturated fat was vindicated, sugar (specifically fructose) took its place.

Since that point, research has been coming out showing that sugar is capable of increasing all these makers in much the same way (1).

But as we found out with saturated fat, just because something elevates those markers under certain circumstances doesn’t mean that it’s causing the chronic conditions that also show elevated levels of those markers.

And it’s more than just that.

The research showing that sugar causes inflammation can’t be extrapolated to real-world applications with human beings for 3 reasons:

  1. We’re not rats
  2. We have self-regulating sugar consumption mechanisms
  3. Sugar’s inflammatory effects require more than just sugar

Let’s break these reasons down one by one.

 

1. We’re not rats

Rats are useful model organisms because their physiology is similar to ours. But, the ability to use sugar seems to be one way that we differ significantly.

Inflammation from sugar/fructose consumption occurs when there’s too much fructose for the liver to effectively handle. At this point, the liver converts more of the fructose to triglycerides (fat) and fructose and its metabolites build up, which triggers inflammation.

For this reason, the conversion of fructose to fat in the liver is a good marker for inflammation.

But, when rats consume fructose, their livers convert many times more of it to fat than our livers do (2, 3, 4, 5).

Because sugar and fructose’s effects are dose-dependent, this difference has HUGE implications for whether sugar causes inflammation in humans! So huge, in fact, that rats are considered extremely poor models for studying fructose’s effects on the human liver (5).

But, almost all the research suggesting that sugar causes inflammation is done on rats! When research has been done to try to show this inflammation in humans, it’s only showcased our livers’ incredible ability to handle fructose.

Our livers hardly convert any fructose to fat because they oxidize (burn), store, or share almost all of it (6, 7, 8, 9, 10, 11, 12, 13, 14, 15). It takes extremely large quantities of sugar, around as much as in 40 cans of soda over 2 days, for our livers to convert appreciable amounts of fructose to fat (13).

In other words, the fact that a high-fructose diet increases inflammation in rats does NOT mean that it does in humans, and it would take massive amounts of fructose to have those same inflammatory effects.

 

2. We have self-regulating sugar consumption mechanisms

One of the arguments for sugar causing inflammation is that it doesn’t satisfy us and keeps us hungry so that we eat too much of it. And that may be true, to a point. Although, eating more is certainly not a problem on its own (why “eat less and exercise more” is the worst advice for fat loss and health).

However, this argument falls short because the most important regulator of the amount of food we eat isn’t accounted for: energy.

The energy status of the liver and hypothalamus (a part of our brain) regulates the amount of food we eat (16, 17). When they don’t have enough energy, we feel hungry. And when they do have enough energy, we feel satisfied.

And guess what increases the energy of our livers and hypothalamus the most…

That’s right, sugar!

In other words, we won’t eat too much sugar as long as our bodies can use the sugar to produce energy.

 

3. Sugar’s inflammatory effects require more than just sugar

One of the many things that can inhibit energy production is polyunsaturated fats, or PUFA. But, PUFA do more than just inhibit energy production – they play a major role in inflammation.

When rats are given extremely large amounts of fructose, the JNK pathway is activated which causes inflammation. But, this pathway isn’t activated if the metabolites of PUFA are blocked, even in the presence of excessive amounts of fructose (18).

Instead, the rats appear to be the same as rats that aren’t fed excessive amounts of fructose and don’t produce large amounts of triglycerides. This suggests that the metabolites of PUFA interfere with the oxidation or storage of fructose, causing more fructose to be converted to fat.

So, the fact that rats are typically fed high-PUFA diets may also play a role in the inflammation seen when they’re given excessive amounts of fructose.

 

The Sweet Truth About Inflammation

Unless you’re eating HUGE quantities of sugar, your body can’t properly use sugar, or you’re a rat, you don’t need to worry about sugar causing inflammation.

As I mentioned in part 1, sugar (particularly fructose) has many benefits, including fueling the liver and the brain. Fructose even has anti-inflammatory and antioxidant effects (20, 21), and when given in normal amounts it actually inhibits the exact inflammatory pathways that it activates when given to rats in huge amounts (22).

But I will remind you that this doesn’t mean that all foods that have sugar are beneficial!

What it does mean is that just because a food contains sugar doesn’t mean it’s unhealthy, and we don’t have to avoid foods simply because of their sugar content.

 

References

Sugar Does NOT Cause Inflammation (Part 2)

In part 1 of this series, I explained some of the basic physiology underlying what happens when we consume sugar. I also explained why, while sugar can cause inflammation, it takes A LOT of sugar and the inflammation it causes isn’t necessarily harmful.

In this article, I’m going to explore this topic a little more in depth and explain why the research behind sugar causing inflammation is so misleading.

But before we dive into the research I’d like to first mention that I’m not going to include observational studies (association-based population studies).

There are many confounding variables in these types of studies, the biggest one being that sugar is widely considered unhealthy. So, those that consume more sugar typically care less about their health and do other unhealthy things. And the opposite is true for those who consume less sugar. (How many people do you know who try to be healthy but also drink soda every day and have doughnuts for breakfast?)

Those studies aside, there are many research studies that conclude that sugar, specifically fructose, causes inflammation. So, let’s start there.

 

Research Shows That Sugar Causes Inflammation

In chronic conditions like diabetes, heart disease, cancer, autoimmune conditions, and obesity, several markers are elevated that indicate chronic inflammation: triglycerides, free fatty acids, fasting blood glucose, fasting insulin, blood pressure, cholesterol, LDL, VLDL, TNF-a, NF-kb, IL-6, etc.

These markers are all symptoms of an inability to produce energy, which ends up causing the perpetual damage that we associate with these conditions.

For many decades, saturated fat was blamed for causing these conditions and was shown to increase these markers. But after saturated fat was vindicated, sugar (specifically fructose) took its place.

Since that point, research has been coming out showing that sugar is capable of increasing all these makers in much the same way (1).

But as we found out with saturated fat, just because something elevates those markers under certain circumstances doesn’t mean that it’s causing the chronic conditions that also show elevated levels of those markers.

And it’s more than just that.

The research showing that sugar causes inflammation can’t be extrapolated to real-world applications with human beings for 3 reasons:

  1. We’re not rats
  2. We have self-regulating sugar consumption mechanisms
  3. Sugar’s inflammatory effects require more than just sugar

Let’s break these reasons down one by one.

 

1. We’re not rats

Rats are useful model organisms because their physiology is similar to ours. But, the ability to use sugar seems to be one way that we differ significantly.

Inflammation from sugar/fructose consumption occurs when there’s too much fructose for the liver to effectively handle. At this point, the liver converts more of the fructose to triglycerides (fat) and fructose and its metabolites build up, which triggers inflammation.

For this reason, the conversion of fructose to fat in the liver is a good marker for inflammation.

But, when rats consume fructose, their livers convert many times more of it to fat than our livers do (2, 3, 4, 5).

Because sugar and fructose’s effects are dose-dependent, this difference has HUGE implications for whether sugar causes inflammation in humans! So huge, in fact, that rats are considered extremely poor models for studying fructose’s effects on the human liver (5).

But, almost all the research suggesting that sugar causes inflammation is done on rats! When research has been done to try to show this inflammation in humans, it’s only showcased our livers’ incredible ability to handle fructose.

Our livers hardly convert any fructose to fat because they oxidize (burn), store, or share almost all of it (6, 7, 8, 9, 10, 11, 12, 13, 14, 15). It takes extremely large quantities of sugar, around as much as in 40 cans of soda over 2 days, for our livers to convert appreciable amounts of fructose to fat (13).

In other words, the fact that a high-fructose diet increases inflammation in rats does NOT mean that it does in humans, and it would take massive amounts of fructose to have those same inflammatory effects.

 

2. We have self-regulating sugar consumption mechanisms

One of the arguments for sugar causing inflammation is that it doesn’t satisfy us and keeps us hungry so that we eat too much of it. And that may be true, to a point. Although, eating more is certainly not a problem on its own (why “eat less and exercise more” is the worst advice for fat loss and health).

However, this argument falls short because the most important regulator of the amount of food we eat isn’t accounted for: energy.

The energy status of the liver and hypothalamus (a part of our brain) regulates the amount of food we eat (16, 17). When they don’t have enough energy, we feel hungry. And when they do have enough energy, we feel satisfied.

And guess what increases the energy of our livers and hypothalamus the most…

That’s right, sugar!

In other words, we won’t eat too much sugar as long as our bodies can use the sugar to produce energy.

 

3. Sugar’s inflammatory effects require more than just sugar

One of the many things that can inhibit energy production is polyunsaturated fats, or PUFA. But, PUFA do more than just inhibit energy production – they play a major role in inflammation.

When rats are given extremely large amounts of fructose, the JNK pathway is activated which causes inflammation. But, this pathway isn’t activated if the metabolites of PUFA are blocked, even in the presence of excessive amounts of fructose (18).

Instead, the rats appear to be the same as rats that aren’t fed excessive amounts of fructose and don’t produce large amounts of triglycerides. This suggests that the metabolites of PUFA interfere with the oxidation or storage of fructose, causing more fructose to be converted to fat.

So, the fact that rats are typically fed high-PUFA diets may also play a role in the inflammation seen when they’re given excessive amounts of fructose.

 

The Sweet Truth About Inflammation

Unless you’re eating HUGE quantities of sugar, your body can’t properly use sugar, or you’re a rat, you don’t need to worry about sugar causing inflammation.

As I mentioned in part 1, sugar (particularly fructose) has many benefits, including fueling the liver and the brain. Fructose even has anti-inflammatory and antioxidant effects (20, 21), and when given in normal amounts it actually inhibits the exact inflammatory pathways that it activates when given to rats in huge amounts (22).

But I will remind you that this doesn’t mean that all foods that have sugar are beneficial!

What it does mean is that just because a food contains sugar doesn’t mean it’s unhealthy, and we don’t have to avoid foods simply because of their sugar content.

 

References

Sugar Does NOT Cause Inflammation (Part 2)

In part 1 of this series, I explained some of the basic physiology underlying what happens when we consume sugar. I also explained why, while sugar can cause inflammation, it takes A LOT of sugar and the inflammation it causes isn’t necessarily harmful.

In this article, I’m going to explore this topic a little more in depth and explain why the research behind sugar causing inflammation is so misleading.

But before we dive into the research I’d like to first mention that I’m not going to include observational studies (association-based population studies).

There are many confounding variables in these types of studies, the biggest one being that sugar is widely considered unhealthy. So, those that consume more sugar typically care less about their health and do other unhealthy things. And the opposite is true for those who consume less sugar. (How many people do you know who try to be healthy but also drink soda every day and have doughnuts for breakfast?)

Those studies aside, there are many research studies that conclude that sugar, specifically fructose, causes inflammation. So, let’s start there.

 

Research Shows That Sugar Causes Inflammation

In chronic conditions like diabetes, heart disease, cancer, autoimmune conditions, and obesity, several markers are elevated that indicate chronic inflammation: triglycerides, free fatty acids, fasting blood glucose, fasting insulin, blood pressure, cholesterol, LDL, VLDL, TNF-a, NF-kb, IL-6, etc.

These markers are all symptoms of an inability to produce energy, which ends up causing the perpetual damage that we associate with these conditions.

For many decades, saturated fat was blamed for causing these conditions and was shown to increase these markers. But after saturated fat was vindicated, sugar (specifically fructose) took its place.

Since that point, research has been coming out showing that sugar is capable of increasing all these makers in much the same way (1).

But as we found out with saturated fat, just because something elevates those markers under certain circumstances doesn’t mean that it’s causing the chronic conditions that also show elevated levels of those markers.

And it’s more than just that.

The research showing that sugar causes inflammation can’t be extrapolated to real-world applications with human beings for 3 reasons:

  1. We’re not rats
  2. We have self-regulating sugar consumption mechanisms
  3. Sugar’s inflammatory effects require more than just sugar

Let’s break these reasons down one by one.

 

1. We’re not rats

Rats are useful model organisms because their physiology is similar to ours. But, the ability to use sugar seems to be one way that we differ significantly.

Inflammation from sugar/fructose consumption occurs when there’s too much fructose for the liver to effectively handle. At this point, the liver converts more of the fructose to triglycerides (fat) and fructose and its metabolites build up, which triggers inflammation.

For this reason, the conversion of fructose to fat in the liver is a good marker for inflammation.

But, when rats consume fructose, their livers convert many times more of it to fat than our livers do (2, 3, 4, 5).

Because sugar and fructose’s effects are dose-dependent, this difference has HUGE implications for whether sugar causes inflammation in humans! So huge, in fact, that rats are considered extremely poor models for studying fructose’s effects on the human liver (5).

But, almost all the research suggesting that sugar causes inflammation is done on rats! When research has been done to try to show this inflammation in humans, it’s only showcased our livers’ incredible ability to handle fructose.

Our livers hardly convert any fructose to fat because they oxidize (burn), store, or share almost all of it (6, 7, 8, 9, 10, 11, 12, 13, 14, 15). It takes extremely large quantities of sugar, around as much as in 40 cans of soda over 2 days, for our livers to convert appreciable amounts of fructose to fat (13).

In other words, the fact that a high-fructose diet increases inflammation in rats does NOT mean that it does in humans, and it would take massive amounts of fructose to have those same inflammatory effects.

 

2. We have self-regulating sugar consumption mechanisms

One of the arguments for sugar causing inflammation is that it doesn’t satisfy us and keeps us hungry so that we eat too much of it. And that may be true, to a point. Although, eating more is certainly not a problem on its own (why “eat less and exercise more” is the worst advice for fat loss and health).

However, this argument falls short because the most important regulator of the amount of food we eat isn’t accounted for: energy.

The energy status of the liver and hypothalamus (a part of our brain) regulates the amount of food we eat (16, 17). When they don’t have enough energy, we feel hungry. And when they do have enough energy, we feel satisfied.

And guess what increases the energy of our livers and hypothalamus the most…

That’s right, sugar!

In other words, we won’t eat too much sugar as long as our bodies can use the sugar to produce energy.

 

3. Sugar’s inflammatory effects require more than just sugar

One of the many things that can inhibit energy production is polyunsaturated fats, or PUFA. But, PUFA do more than just inhibit energy production – they play a major role in inflammation.

When rats are given extremely large amounts of fructose, the JNK pathway is activated which causes inflammation. But, this pathway isn’t activated if the metabolites of PUFA are blocked, even in the presence of excessive amounts of fructose (18).

Instead, the rats appear to be the same as rats that aren’t fed excessive amounts of fructose and don’t produce large amounts of triglycerides. This suggests that the metabolites of PUFA interfere with the oxidation or storage of fructose, causing more fructose to be converted to fat.

So, the fact that rats are typically fed high-PUFA diets may also play a role in the inflammation seen when they’re given excessive amounts of fructose.

 

The Sweet Truth About Inflammation

Unless you’re eating HUGE quantities of sugar, your body can’t properly use sugar, or you’re a rat, you don’t need to worry about sugar causing inflammation.

As I mentioned in part 1, sugar (particularly fructose) has many benefits, including fueling the liver and the brain. Fructose even has anti-inflammatory and antioxidant effects (20, 21), and when given in normal amounts it actually inhibits the exact inflammatory pathways that it activates when given to rats in huge amounts (22).

But I will remind you that this doesn’t mean that all foods that have sugar are beneficial!

What it does mean is that just because a food contains sugar doesn’t mean it’s unhealthy, and we don’t have to avoid foods simply because of their sugar content.

 

References

Sugar Does NOT Cause Inflammation (Part 2)

In part 1 of this series, I explained some of the basic physiology underlying what happens when we consume sugar. I also explained why, while sugar can cause inflammation, it takes A LOT of sugar and the inflammation it causes isn’t necessarily harmful.

In this article, I’m going to explore this topic a little more in depth and explain why the research behind sugar causing inflammation is so misleading.

But before we dive into the research I’d like to first mention that I’m not going to include observational studies (association-based population studies).

There are many confounding variables in these types of studies, the biggest one being that sugar is widely considered unhealthy. So, those that consume more sugar typically care less about their health and do other unhealthy things. And the opposite is true for those who consume less sugar. (How many people do you know who try to be healthy but also drink soda every day and have doughnuts for breakfast?)

Those studies aside, there are many research studies that conclude that sugar, specifically fructose, causes inflammation. So, let’s start there.

 

Research Shows That Sugar Causes Inflammation

In chronic conditions like diabetes, heart disease, cancer, autoimmune conditions, and obesity, several markers are elevated that indicate chronic inflammation: triglycerides, free fatty acids, fasting blood glucose, fasting insulin, blood pressure, cholesterol, LDL, VLDL, TNF-a, NF-kb, IL-6, etc.

These markers are all symptoms of an inability to produce energy, which ends up causing the perpetual damage that we associate with these conditions.

For many decades, saturated fat was blamed for causing these conditions and was shown to increase these markers. But after saturated fat was vindicated, sugar (specifically fructose) took its place.

Since that point, research has been coming out showing that sugar is capable of increasing all these makers in much the same way (1).

But as we found out with saturated fat, just because something elevates those markers under certain circumstances doesn’t mean that it’s causing the chronic conditions that also show elevated levels of those markers.

And it’s more than just that.

The research showing that sugar causes inflammation can’t be extrapolated to real-world applications with human beings for 3 reasons:

  1. We’re not rats
  2. We have self-regulating sugar consumption mechanisms
  3. Sugar’s inflammatory effects require more than just sugar

Let’s break these reasons down one by one.

 

1. We’re not rats

Rats are useful model organisms because their physiology is similar to ours. But, the ability to use sugar seems to be one way that we differ significantly.

Inflammation from sugar/fructose consumption occurs when there’s too much fructose for the liver to effectively handle. At this point, the liver converts more of the fructose to triglycerides (fat) and fructose and its metabolites build up, which triggers inflammation.

For this reason, the conversion of fructose to fat in the liver is a good marker for inflammation.

But, when rats consume fructose, their livers convert many times more of it to fat than our livers do (2, 3, 4, 5).

Because sugar and fructose’s effects are dose-dependent, this difference has HUGE implications for whether sugar causes inflammation in humans! So huge, in fact, that rats are considered extremely poor models for studying fructose’s effects on the human liver (5).

But, almost all the research suggesting that sugar causes inflammation is done on rats! When research has been done to try to show this inflammation in humans, it’s only showcased our livers’ incredible ability to handle fructose.

Our livers hardly convert any fructose to fat because they oxidize (burn), store, or share almost all of it (6, 7, 8, 9, 10, 11, 12, 13, 14, 15). It takes extremely large quantities of sugar, around as much as in 40 cans of soda over 2 days, for our livers to convert appreciable amounts of fructose to fat (13).

In other words, the fact that a high-fructose diet increases inflammation in rats does NOT mean that it does in humans, and it would take massive amounts of fructose to have those same inflammatory effects.

 

2. We have self-regulating sugar consumption mechanisms

One of the arguments for sugar causing inflammation is that it doesn’t satisfy us and keeps us hungry so that we eat too much of it. And that may be true, to a point. Although, eating more is certainly not a problem on its own (why “eat less and exercise more” is the worst advice for fat loss and health).

However, this argument falls short because the most important regulator of the amount of food we eat isn’t accounted for: energy.

The energy status of the liver and hypothalamus (a part of our brain) regulates the amount of food we eat (16, 17). When they don’t have enough energy, we feel hungry. And when they do have enough energy, we feel satisfied.

And guess what increases the energy of our livers and hypothalamus the most…

That’s right, sugar!

In other words, we won’t eat too much sugar as long as our bodies can use the sugar to produce energy.

 

3. Sugar’s inflammatory effects require more than just sugar

One of the many things that can inhibit energy production is polyunsaturated fats, or PUFA. But, PUFA do more than just inhibit energy production – they play a major role in inflammation.

When rats are given extremely large amounts of fructose, the JNK pathway is activated which causes inflammation. But, this pathway isn’t activated if the metabolites of PUFA are blocked, even in the presence of excessive amounts of fructose (18).

Instead, the rats appear to be the same as rats that aren’t fed excessive amounts of fructose and don’t produce large amounts of triglycerides. This suggests that the metabolites of PUFA interfere with the oxidation or storage of fructose, causing more fructose to be converted to fat.

So, the fact that rats are typically fed high-PUFA diets may also play a role in the inflammation seen when they’re given excessive amounts of fructose.

 

The Sweet Truth About Inflammation

Unless you’re eating HUGE quantities of sugar, your body can’t properly use sugar, or you’re a rat, you don’t need to worry about sugar causing inflammation.

As I mentioned in part 1, sugar (particularly fructose) has many benefits, including fueling the liver and the brain. Fructose even has anti-inflammatory and antioxidant effects (20, 21), and when given in normal amounts it actually inhibits the exact inflammatory pathways that it activates when given to rats in huge amounts (22).

But I will remind you that this doesn’t mean that all foods that have sugar are beneficial!

What it does mean is that just because a food contains sugar doesn’t mean it’s unhealthy, and we don’t have to avoid foods simply because of their sugar content.

 

References

Sugar Does NOT Cause Inflammation (Part 2)

In part 1 of this series, I explained some of the basic physiology underlying what happens when we consume sugar. I also explained why, while sugar can cause inflammation, it takes A LOT of sugar and the inflammation it causes isn’t necessarily harmful.

In this article, I’m going to explore this topic a little more in depth and explain why the research behind sugar causing inflammation is so misleading.

But before we dive into the research I’d like to first mention that I’m not going to include observational studies (association-based population studies).

There are many confounding variables in these types of studies, the biggest one being that sugar is widely considered unhealthy. So, those that consume more sugar typically care less about their health and do other unhealthy things. And the opposite is true for those who consume less sugar. (How many people do you know who try to be healthy but also drink soda every day and have doughnuts for breakfast?)

Those studies aside, there are many research studies that conclude that sugar, specifically fructose, causes inflammation. So, let’s start there.

 

Research Shows That Sugar Causes Inflammation

In chronic conditions like diabetes, heart disease, cancer, autoimmune conditions, and obesity, several markers are elevated that indicate chronic inflammation: triglycerides, free fatty acids, fasting blood glucose, fasting insulin, blood pressure, cholesterol, LDL, VLDL, TNF-a, NF-kb, IL-6, etc.

These markers are all symptoms of an inability to produce energy, which ends up causing the perpetual damage that we associate with these conditions.

For many decades, saturated fat was blamed for causing these conditions and was shown to increase these markers. But after saturated fat was vindicated, sugar (specifically fructose) took its place.

Since that point, research has been coming out showing that sugar is capable of increasing all these makers in much the same way (1).

But as we found out with saturated fat, just because something elevates those markers under certain circumstances doesn’t mean that it’s causing the chronic conditions that also show elevated levels of those markers.

And it’s more than just that.

The research showing that sugar causes inflammation can’t be extrapolated to real-world applications with human beings for 3 reasons:

  1. We’re not rats
  2. We have self-regulating sugar consumption mechanisms
  3. Sugar’s inflammatory effects require more than just sugar

Let’s break these reasons down one by one.

 

1. We’re not rats

Rats are useful model organisms because their physiology is similar to ours. But, the ability to use sugar seems to be one way that we differ significantly.

Inflammation from sugar/fructose consumption occurs when there’s too much fructose for the liver to effectively handle. At this point, the liver converts more of the fructose to triglycerides (fat) and fructose and its metabolites build up, which triggers inflammation.

For this reason, the conversion of fructose to fat in the liver is a good marker for inflammation.

But, when rats consume fructose, their livers convert many times more of it to fat than our livers do (2, 3, 4, 5).

Because sugar and fructose’s effects are dose-dependent, this difference has HUGE implications for whether sugar causes inflammation in humans! So huge, in fact, that rats are considered extremely poor models for studying fructose’s effects on the human liver (5).

But, almost all the research suggesting that sugar causes inflammation is done on rats! When research has been done to try to show this inflammation in humans, it’s only showcased our livers’ incredible ability to handle fructose.

Our livers hardly convert any fructose to fat because they oxidize (burn), store, or share almost all of it (6, 7, 8, 9, 10, 11, 12, 13, 14, 15). It takes extremely large quantities of sugar, around as much as in 40 cans of soda over 2 days, for our livers to convert appreciable amounts of fructose to fat (13).

In other words, the fact that a high-fructose diet increases inflammation in rats does NOT mean that it does in humans, and it would take massive amounts of fructose to have those same inflammatory effects.

 

2. We have self-regulating sugar consumption mechanisms

One of the arguments for sugar causing inflammation is that it doesn’t satisfy us and keeps us hungry so that we eat too much of it. And that may be true, to a point. Although, eating more is certainly not a problem on its own (why “eat less and exercise more” is the worst advice for fat loss and health).

However, this argument falls short because the most important regulator of the amount of food we eat isn’t accounted for: energy.

The energy status of the liver and hypothalamus (a part of our brain) regulates the amount of food we eat (16, 17). When they don’t have enough energy, we feel hungry. And when they do have enough energy, we feel satisfied.

And guess what increases the energy of our livers and hypothalamus the most…

That’s right, sugar!

In other words, we won’t eat too much sugar as long as our bodies can use the sugar to produce energy.

 

3. Sugar’s inflammatory effects require more than just sugar

One of the many things that can inhibit energy production is polyunsaturated fats, or PUFA. But, PUFA do more than just inhibit energy production – they play a major role in inflammation.

When rats are given extremely large amounts of fructose, the JNK pathway is activated which causes inflammation. But, this pathway isn’t activated if the metabolites of PUFA are blocked, even in the presence of excessive amounts of fructose (18).

Instead, the rats appear to be the same as rats that aren’t fed excessive amounts of fructose and don’t produce large amounts of triglycerides. This suggests that the metabolites of PUFA interfere with the oxidation or storage of fructose, causing more fructose to be converted to fat.

So, the fact that rats are typically fed high-PUFA diets may also play a role in the inflammation seen when they’re given excessive amounts of fructose.

 

The Sweet Truth About Inflammation

Unless you’re eating HUGE quantities of sugar, your body can’t properly use sugar, or you’re a rat, you don’t need to worry about sugar causing inflammation.

As I mentioned in part 1, sugar (particularly fructose) has many benefits, including fueling the liver and the brain. Fructose even has anti-inflammatory and antioxidant effects (20, 21), and when given in normal amounts it actually inhibits the exact inflammatory pathways that it activates when given to rats in huge amounts (22).

But I will remind you that this doesn’t mean that all foods that have sugar are beneficial!

What it does mean is that just because a food contains sugar doesn’t mean it’s unhealthy, and we don’t have to avoid foods simply because of their sugar content.

 

References

Sugar Does NOT Cause Inflammation (Part 2)

In part 1 of this series, I explained some of the basic physiology underlying what happens when we consume sugar. I also explained why, while sugar can cause inflammation, it takes A LOT of sugar and the inflammation it causes isn’t necessarily harmful.

In this article, I’m going to explore this topic a little more in depth and explain why the research behind sugar causing inflammation is so misleading.

But before we dive into the research I’d like to first mention that I’m not going to include observational studies (association-based population studies).

There are many confounding variables in these types of studies, the biggest one being that sugar is widely considered unhealthy. So, those that consume more sugar typically care less about their health and do other unhealthy things. And the opposite is true for those who consume less sugar. (How many people do you know who try to be healthy but also drink soda every day and have doughnuts for breakfast?)

Those studies aside, there are many research studies that conclude that sugar, specifically fructose, causes inflammation. So, let’s start there.

 

Research Shows That Sugar Causes Inflammation

In chronic conditions like diabetes, heart disease, cancer, autoimmune conditions, and obesity, several markers are elevated that indicate chronic inflammation: triglycerides, free fatty acids, fasting blood glucose, fasting insulin, blood pressure, cholesterol, LDL, VLDL, TNF-a, NF-kb, IL-6, etc.

These markers are all symptoms of an inability to produce energy, which ends up causing the perpetual damage that we associate with these conditions.

For many decades, saturated fat was blamed for causing these conditions and was shown to increase these markers. But after saturated fat was vindicated, sugar (specifically fructose) took its place.

Since that point, research has been coming out showing that sugar is capable of increasing all these makers in much the same way (1).

But as we found out with saturated fat, just because something elevates those markers under certain circumstances doesn’t mean that it’s causing the chronic conditions that also show elevated levels of those markers.

And it’s more than just that.

The research showing that sugar causes inflammation can’t be extrapolated to real-world applications with human beings for 3 reasons:

  1. We’re not rats
  2. We have self-regulating sugar consumption mechanisms
  3. Sugar’s inflammatory effects require more than just sugar

Let’s break these reasons down one by one.

 

1. We’re not rats

Rats are useful model organisms because their physiology is similar to ours. But, the ability to use sugar seems to be one way that we differ significantly.

Inflammation from sugar/fructose consumption occurs when there’s too much fructose for the liver to effectively handle. At this point, the liver converts more of the fructose to triglycerides (fat) and fructose and its metabolites build up, which triggers inflammation.

For this reason, the conversion of fructose to fat in the liver is a good marker for inflammation.

But, when rats consume fructose, their livers convert many times more of it to fat than our livers do (2, 3, 4, 5).

Because sugar and fructose’s effects are dose-dependent, this difference has HUGE implications for whether sugar causes inflammation in humans! So huge, in fact, that rats are considered extremely poor models for studying fructose’s effects on the human liver (5).

But, almost all the research suggesting that sugar causes inflammation is done on rats! When research has been done to try to show this inflammation in humans, it’s only showcased our livers’ incredible ability to handle fructose.

Our livers hardly convert any fructose to fat because they oxidize (burn), store, or share almost all of it (6, 7, 8, 9, 10, 11, 12, 13, 14, 15). It takes extremely large quantities of sugar, around as much as in 40 cans of soda over 2 days, for our livers to convert appreciable amounts of fructose to fat (13).

In other words, the fact that a high-fructose diet increases inflammation in rats does NOT mean that it does in humans, and it would take massive amounts of fructose to have those same inflammatory effects.

 

2. We have self-regulating sugar consumption mechanisms

One of the arguments for sugar causing inflammation is that it doesn’t satisfy us and keeps us hungry so that we eat too much of it. And that may be true, to a point. Although, eating more is certainly not a problem on its own (why “eat less and exercise more” is the worst advice for fat loss and health).

However, this argument falls short because the most important regulator of the amount of food we eat isn’t accounted for: energy.

The energy status of the liver and hypothalamus (a part of our brain) regulates the amount of food we eat (16, 17). When they don’t have enough energy, we feel hungry. And when they do have enough energy, we feel satisfied.

And guess what increases the energy of our livers and hypothalamus the most…

That’s right, sugar!

In other words, we won’t eat too much sugar as long as our bodies can use the sugar to produce energy.

 

3. Sugar’s inflammatory effects require more than just sugar

One of the many things that can inhibit energy production is polyunsaturated fats, or PUFA. But, PUFA do more than just inhibit energy production – they play a major role in inflammation.

When rats are given extremely large amounts of fructose, the JNK pathway is activated which causes inflammation. But, this pathway isn’t activated if the metabolites of PUFA are blocked, even in the presence of excessive amounts of fructose (18).

Instead, the rats appear to be the same as rats that aren’t fed excessive amounts of fructose and don’t produce large amounts of triglycerides. This suggests that the metabolites of PUFA interfere with the oxidation or storage of fructose, causing more fructose to be converted to fat.

So, the fact that rats are typically fed high-PUFA diets may also play a role in the inflammation seen when they’re given excessive amounts of fructose.

 

The Sweet Truth About Inflammation

Unless you’re eating HUGE quantities of sugar, your body can’t properly use sugar, or you’re a rat, you don’t need to worry about sugar causing inflammation.

As I mentioned in part 1, sugar (particularly fructose) has many benefits, including fueling the liver and the brain. Fructose even has anti-inflammatory and antioxidant effects (20, 21), and when given in normal amounts it actually inhibits the exact inflammatory pathways that it activates when given to rats in huge amounts (22).

But I will remind you that this doesn’t mean that all foods that have sugar are beneficial!

What it does mean is that just because a food contains sugar doesn’t mean it’s unhealthy, and we don’t have to avoid foods simply because of their sugar content.

 

References

Sugar Does NOT Cause Inflammation (Part 2)

In part 1 of this series, I explained some of the basic physiology underlying what happens when we consume sugar. I also explained why, while sugar can cause inflammation, it takes A LOT of sugar and the inflammation it causes isn’t necessarily harmful.

In this article, I’m going to explore this topic a little more in depth and explain why the research behind sugar causing inflammation is so misleading.

But before we dive into the research I’d like to first mention that I’m not going to include observational studies (association-based population studies).

There are many confounding variables in these types of studies, the biggest one being that sugar is widely considered unhealthy. So, those that consume more sugar typically care less about their health and do other unhealthy things. And the opposite is true for those who consume less sugar. (How many people do you know who try to be healthy but also drink soda every day and have doughnuts for breakfast?)

Those studies aside, there are many research studies that conclude that sugar, specifically fructose, causes inflammation. So, let’s start there.

 

Research Shows That Sugar Causes Inflammation

In chronic conditions like diabetes, heart disease, cancer, autoimmune conditions, and obesity, several markers are elevated that indicate chronic inflammation: triglycerides, free fatty acids, fasting blood glucose, fasting insulin, blood pressure, cholesterol, LDL, VLDL, TNF-a, NF-kb, IL-6, etc.

These markers are all symptoms of an inability to produce energy, which ends up causing the perpetual damage that we associate with these conditions.

For many decades, saturated fat was blamed for causing these conditions and was shown to increase these markers. But after saturated fat was vindicated, sugar (specifically fructose) took its place.

Since that point, research has been coming out showing that sugar is capable of increasing all these makers in much the same way (1).

But as we found out with saturated fat, just because something elevates those markers under certain circumstances doesn’t mean that it’s causing the chronic conditions that also show elevated levels of those markers.

And it’s more than just that.

The research showing that sugar causes inflammation can’t be extrapolated to real-world applications with human beings for 3 reasons:

  1. We’re not rats
  2. We have self-regulating sugar consumption mechanisms
  3. Sugar’s inflammatory effects require more than just sugar

Let’s break these reasons down one by one.

 

1. We’re not rats

Rats are useful model organisms because their physiology is similar to ours. But, the ability to use sugar seems to be one way that we differ significantly.

Inflammation from sugar/fructose consumption occurs when there’s too much fructose for the liver to effectively handle. At this point, the liver converts more of the fructose to triglycerides (fat) and fructose and its metabolites build up, which triggers inflammation.

For this reason, the conversion of fructose to fat in the liver is a good marker for inflammation.

But, when rats consume fructose, their livers convert many times more of it to fat than our livers do (2, 3, 4, 5).

Because sugar and fructose’s effects are dose-dependent, this difference has HUGE implications for whether sugar causes inflammation in humans! So huge, in fact, that rats are considered extremely poor models for studying fructose’s effects on the human liver (5).

But, almost all the research suggesting that sugar causes inflammation is done on rats! When research has been done to try to show this inflammation in humans, it’s only showcased our livers’ incredible ability to handle fructose.

Our livers hardly convert any fructose to fat because they oxidize (burn), store, or share almost all of it (6, 7, 8, 9, 10, 11, 12, 13, 14, 15). It takes extremely large quantities of sugar, around as much as in 40 cans of soda over 2 days, for our livers to convert appreciable amounts of fructose to fat (13).

In other words, the fact that a high-fructose diet increases inflammation in rats does NOT mean that it does in humans, and it would take massive amounts of fructose to have those same inflammatory effects.

 

2. We have self-regulating sugar consumption mechanisms

One of the arguments for sugar causing inflammation is that it doesn’t satisfy us and keeps us hungry so that we eat too much of it. And that may be true, to a point. Although, eating more is certainly not a problem on its own (why “eat less and exercise more” is the worst advice for fat loss and health).

However, this argument falls short because the most important regulator of the amount of food we eat isn’t accounted for: energy.

The energy status of the liver and hypothalamus (a part of our brain) regulates the amount of food we eat (16, 17). When they don’t have enough energy, we feel hungry. And when they do have enough energy, we feel satisfied.

And guess what increases the energy of our livers and hypothalamus the most…

That’s right, sugar!

In other words, we won’t eat too much sugar as long as our bodies can use the sugar to produce energy.

 

3. Sugar’s inflammatory effects require more than just sugar

One of the many things that can inhibit energy production is polyunsaturated fats, or PUFA. But, PUFA do more than just inhibit energy production – they play a major role in inflammation.

When rats are given extremely large amounts of fructose, the JNK pathway is activated which causes inflammation. But, this pathway isn’t activated if the metabolites of PUFA are blocked, even in the presence of excessive amounts of fructose (18).

Instead, the rats appear to be the same as rats that aren’t fed excessive amounts of fructose and don’t produce large amounts of triglycerides. This suggests that the metabolites of PUFA interfere with the oxidation or storage of fructose, causing more fructose to be converted to fat.

So, the fact that rats are typically fed high-PUFA diets may also play a role in the inflammation seen when they’re given excessive amounts of fructose.

 

The Sweet Truth About Inflammation

Unless you’re eating HUGE quantities of sugar, your body can’t properly use sugar, or you’re a rat, you don’t need to worry about sugar causing inflammation.

As I mentioned in part 1, sugar (particularly fructose) has many benefits, including fueling the liver and the brain. Fructose even has anti-inflammatory and antioxidant effects (20, 21), and when given in normal amounts it actually inhibits the exact inflammatory pathways that it activates when given to rats in huge amounts (22).

But I will remind you that this doesn’t mean that all foods that have sugar are beneficial!

What it does mean is that just because a food contains sugar doesn’t mean it’s unhealthy, and we don’t have to avoid foods simply because of their sugar content.

 

References

Sugar Does NOT Cause Inflammation (Part 2)

In part 1 of this series, I explained some of the basic physiology underlying what happens when we consume sugar. I also explained why, while sugar can cause inflammation, it takes A LOT of sugar and the inflammation it causes isn’t necessarily harmful.

In this article, I’m going to explore this topic a little more in depth and explain why the research behind sugar causing inflammation is so misleading.

But before we dive into the research I’d like to first mention that I’m not going to include observational studies (association-based population studies).

There are many confounding variables in these types of studies, the biggest one being that sugar is widely considered unhealthy. So, those that consume more sugar typically care less about their health and do other unhealthy things. And the opposite is true for those who consume less sugar. (How many people do you know who try to be healthy but also drink soda every day and have doughnuts for breakfast?)

Those studies aside, there are many research studies that conclude that sugar, specifically fructose, causes inflammation. So, let’s start there.

 

Research Shows That Sugar Causes Inflammation

In chronic conditions like diabetes, heart disease, cancer, autoimmune conditions, and obesity, several markers are elevated that indicate chronic inflammation: triglycerides, free fatty acids, fasting blood glucose, fasting insulin, blood pressure, cholesterol, LDL, VLDL, TNF-a, NF-kb, IL-6, etc.

These markers are all symptoms of an inability to produce energy, which ends up causing the perpetual damage that we associate with these conditions.

For many decades, saturated fat was blamed for causing these conditions and was shown to increase these markers. But after saturated fat was vindicated, sugar (specifically fructose) took its place.

Since that point, research has been coming out showing that sugar is capable of increasing all these makers in much the same way (1).

But as we found out with saturated fat, just because something elevates those markers under certain circumstances doesn’t mean that it’s causing the chronic conditions that also show elevated levels of those markers.

And it’s more than just that.

The research showing that sugar causes inflammation can’t be extrapolated to real-world applications with human beings for 3 reasons:

  1. We’re not rats
  2. We have self-regulating sugar consumption mechanisms
  3. Sugar’s inflammatory effects require more than just sugar

Let’s break these reasons down one by one.

 

1. We’re not rats

Rats are useful model organisms because their physiology is similar to ours. But, the ability to use sugar seems to be one way that we differ significantly.

Inflammation from sugar/fructose consumption occurs when there’s too much fructose for the liver to effectively handle. At this point, the liver converts more of the fructose to triglycerides (fat) and fructose and its metabolites build up, which triggers inflammation.

For this reason, the conversion of fructose to fat in the liver is a good marker for inflammation.

But, when rats consume fructose, their livers convert many times more of it to fat than our livers do (2, 3, 4, 5).

Because sugar and fructose’s effects are dose-dependent, this difference has HUGE implications for whether sugar causes inflammation in humans! So huge, in fact, that rats are considered extremely poor models for studying fructose’s effects on the human liver (5).

But, almost all the research suggesting that sugar causes inflammation is done on rats! When research has been done to try to show this inflammation in humans, it’s only showcased our livers’ incredible ability to handle fructose.

Our livers hardly convert any fructose to fat because they oxidize (burn), store, or share almost all of it (6, 7, 8, 9, 10, 11, 12, 13, 14, 15). It takes extremely large quantities of sugar, around as much as in 40 cans of soda over 2 days, for our livers to convert appreciable amounts of fructose to fat (13).

In other words, the fact that a high-fructose diet increases inflammation in rats does NOT mean that it does in humans, and it would take massive amounts of fructose to have those same inflammatory effects.

 

2. We have self-regulating sugar consumption mechanisms

One of the arguments for sugar causing inflammation is that it doesn’t satisfy us and keeps us hungry so that we eat too much of it. And that may be true, to a point. Although, eating more is certainly not a problem on its own (why “eat less and exercise more” is the worst advice for fat loss and health).

However, this argument falls short because the most important regulator of the amount of food we eat isn’t accounted for: energy.

The energy status of the liver and hypothalamus (a part of our brain) regulates the amount of food we eat (16, 17). When they don’t have enough energy, we feel hungry. And when they do have enough energy, we feel satisfied.

And guess what increases the energy of our livers and hypothalamus the most…

That’s right, sugar!

In other words, we won’t eat too much sugar as long as our bodies can use the sugar to produce energy.

 

3. Sugar’s inflammatory effects require more than just sugar

One of the many things that can inhibit energy production is polyunsaturated fats, or PUFA. But, PUFA do more than just inhibit energy production – they play a major role in inflammation.

When rats are given extremely large amounts of fructose, the JNK pathway is activated which causes inflammation. But, this pathway isn’t activated if the metabolites of PUFA are blocked, even in the presence of excessive amounts of fructose (18).

Instead, the rats appear to be the same as rats that aren’t fed excessive amounts of fructose and don’t produce large amounts of triglycerides. This suggests that the metabolites of PUFA interfere with the oxidation or storage of fructose, causing more fructose to be converted to fat.

So, the fact that rats are typically fed high-PUFA diets may also play a role in the inflammation seen when they’re given excessive amounts of fructose.

 

The Sweet Truth About Inflammation

Unless you’re eating HUGE quantities of sugar, your body can’t properly use sugar, or you’re a rat, you don’t need to worry about sugar causing inflammation.

As I mentioned in part 1, sugar (particularly fructose) has many benefits, including fueling the liver and the brain. Fructose even has anti-inflammatory and antioxidant effects (20, 21), and when given in normal amounts it actually inhibits the exact inflammatory pathways that it activates when given to rats in huge amounts (22).

But I will remind you that this doesn’t mean that all foods that have sugar are beneficial!

What it does mean is that just because a food contains sugar doesn’t mean it’s unhealthy, and we don’t have to avoid foods simply because of their sugar content.

 

References

Sugar Does NOT Cause Inflammation (Part 2)

In part 1 of this series, I explained some of the basic physiology underlying what happens when we consume sugar. I also explained why, while sugar can cause inflammation, it takes A LOT of sugar and the inflammation it causes isn’t necessarily harmful.

In this article, I’m going to explore this topic a little more in depth and explain why the research behind sugar causing inflammation is so misleading.

But before we dive into the research I’d like to first mention that I’m not going to include observational studies (association-based population studies).

There are many confounding variables in these types of studies, the biggest one being that sugar is widely considered unhealthy. So, those that consume more sugar typically care less about their health and do other unhealthy things. And the opposite is true for those who consume less sugar. (How many people do you know who try to be healthy but also drink soda every day and have doughnuts for breakfast?)

Those studies aside, there are many research studies that conclude that sugar, specifically fructose, causes inflammation. So, let’s start there.

 

Research Shows That Sugar Causes Inflammation

In chronic conditions like diabetes, heart disease, cancer, autoimmune conditions, and obesity, several markers are elevated that indicate chronic inflammation: triglycerides, free fatty acids, fasting blood glucose, fasting insulin, blood pressure, cholesterol, LDL, VLDL, TNF-a, NF-kb, IL-6, etc.

These markers are all symptoms of an inability to produce energy, which ends up causing the perpetual damage that we associate with these conditions.

For many decades, saturated fat was blamed for causing these conditions and was shown to increase these markers. But after saturated fat was vindicated, sugar (specifically fructose) took its place.

Since that point, research has been coming out showing that sugar is capable of increasing all these makers in much the same way (1).

But as we found out with saturated fat, just because something elevates those markers under certain circumstances doesn’t mean that it’s causing the chronic conditions that also show elevated levels of those markers.

And it’s more than just that.

The research showing that sugar causes inflammation can’t be extrapolated to real-world applications with human beings for 3 reasons:

  1. We’re not rats
  2. We have self-regulating sugar consumption mechanisms
  3. Sugar’s inflammatory effects require more than just sugar

Let’s break these reasons down one by one.

 

1. We’re not rats

Rats are useful model organisms because their physiology is similar to ours. But, the ability to use sugar seems to be one way that we differ significantly.

Inflammation from sugar/fructose consumption occurs when there’s too much fructose for the liver to effectively handle. At this point, the liver converts more of the fructose to triglycerides (fat) and fructose and its metabolites build up, which triggers inflammation.

For this reason, the conversion of fructose to fat in the liver is a good marker for inflammation.

But, when rats consume fructose, their livers convert many times more of it to fat than our livers do (2, 3, 4, 5).

Because sugar and fructose’s effects are dose-dependent, this difference has HUGE implications for whether sugar causes inflammation in humans! So huge, in fact, that rats are considered extremely poor models for studying fructose’s effects on the human liver (5).

But, almost all the research suggesting that sugar causes inflammation is done on rats! When research has been done to try to show this inflammation in humans, it’s only showcased our livers’ incredible ability to handle fructose.

Our livers hardly convert any fructose to fat because they oxidize (burn), store, or share almost all of it (6, 7, 8, 9, 10, 11, 12, 13, 14, 15). It takes extremely large quantities of sugar, around as much as in 40 cans of soda over 2 days, for our livers to convert appreciable amounts of fructose to fat (13).

In other words, the fact that a high-fructose diet increases inflammation in rats does NOT mean that it does in humans, and it would take massive amounts of fructose to have those same inflammatory effects.

 

2. We have self-regulating sugar consumption mechanisms

One of the arguments for sugar causing inflammation is that it doesn’t satisfy us and keeps us hungry so that we eat too much of it. And that may be true, to a point. Although, eating more is certainly not a problem on its own (why “eat less and exercise more” is the worst advice for fat loss and health).

However, this argument falls short because the most important regulator of the amount of food we eat isn’t accounted for: energy.

The energy status of the liver and hypothalamus (a part of our brain) regulates the amount of food we eat (16, 17). When they don’t have enough energy, we feel hungry. And when they do have enough energy, we feel satisfied.

And guess what increases the energy of our livers and hypothalamus the most…

That’s right, sugar!

In other words, we won’t eat too much sugar as long as our bodies can use the sugar to produce energy.

 

3. Sugar’s inflammatory effects require more than just sugar

One of the many things that can inhibit energy production is polyunsaturated fats, or PUFA. But, PUFA do more than just inhibit energy production – they play a major role in inflammation.

When rats are given extremely large amounts of fructose, the JNK pathway is activated which causes inflammation. But, this pathway isn’t activated if the metabolites of PUFA are blocked, even in the presence of excessive amounts of fructose (18).

Instead, the rats appear to be the same as rats that aren’t fed excessive amounts of fructose and don’t produce large amounts of triglycerides. This suggests that the metabolites of PUFA interfere with the oxidation or storage of fructose, causing more fructose to be converted to fat.

So, the fact that rats are typically fed high-PUFA diets may also play a role in the inflammation seen when they’re given excessive amounts of fructose.

 

The Sweet Truth About Inflammation

Unless you’re eating HUGE quantities of sugar, your body can’t properly use sugar, or you’re a rat, you don’t need to worry about sugar causing inflammation.

As I mentioned in part 1, sugar (particularly fructose) has many benefits, including fueling the liver and the brain. Fructose even has anti-inflammatory and antioxidant effects (20, 21), and when given in normal amounts it actually inhibits the exact inflammatory pathways that it activates when given to rats in huge amounts (22).

But I will remind you that this doesn’t mean that all foods that have sugar are beneficial!

What it does mean is that just because a food contains sugar doesn’t mean it’s unhealthy, and we don’t have to avoid foods simply because of their sugar content.

 

References

Sugar Does NOT Cause Inflammation (Part 2)

In part 1 of this series, I explained some of the basic physiology underlying what happens when we consume sugar. I also explained why, while sugar can cause inflammation, it takes A LOT of sugar and the inflammation it causes isn’t necessarily harmful.

In this article, I’m going to explore this topic a little more in depth and explain why the research behind sugar causing inflammation is so misleading.

But before we dive into the research I’d like to first mention that I’m not going to include observational studies (association-based population studies).

There are many confounding variables in these types of studies, the biggest one being that sugar is widely considered unhealthy. So, those that consume more sugar typically care less about their health and do other unhealthy things. And the opposite is true for those who consume less sugar. (How many people do you know who try to be healthy but also drink soda every day and have doughnuts for breakfast?)

Those studies aside, there are many research studies that conclude that sugar, specifically fructose, causes inflammation. So, let’s start there.

 

Research Shows That Sugar Causes Inflammation

In chronic conditions like diabetes, heart disease, cancer, autoimmune conditions, and obesity, several markers are elevated that indicate chronic inflammation: triglycerides, free fatty acids, fasting blood glucose, fasting insulin, blood pressure, cholesterol, LDL, VLDL, TNF-a, NF-kb, IL-6, etc.

These markers are all symptoms of an inability to produce energy, which ends up causing the perpetual damage that we associate with these conditions.

For many decades, saturated fat was blamed for causing these conditions and was shown to increase these markers. But after saturated fat was vindicated, sugar (specifically fructose) took its place.

Since that point, research has been coming out showing that sugar is capable of increasing all these makers in much the same way (1).

But as we found out with saturated fat, just because something elevates those markers under certain circumstances doesn’t mean that it’s causing the chronic conditions that also show elevated levels of those markers.

And it’s more than just that.

The research showing that sugar causes inflammation can’t be extrapolated to real-world applications with human beings for 3 reasons:

  1. We’re not rats
  2. We have self-regulating sugar consumption mechanisms
  3. Sugar’s inflammatory effects require more than just sugar

Let’s break these reasons down one by one.

 

1. We’re not rats

Rats are useful model organisms because their physiology is similar to ours. But, the ability to use sugar seems to be one way that we differ significantly.

Inflammation from sugar/fructose consumption occurs when there’s too much fructose for the liver to effectively handle. At this point, the liver converts more of the fructose to triglycerides (fat) and fructose and its metabolites build up, which triggers inflammation.

For this reason, the conversion of fructose to fat in the liver is a good marker for inflammation.

But, when rats consume fructose, their livers convert many times more of it to fat than our livers do (2, 3, 4, 5).

Because sugar and fructose’s effects are dose-dependent, this difference has HUGE implications for whether sugar causes inflammation in humans! So huge, in fact, that rats are considered extremely poor models for studying fructose’s effects on the human liver (5).

But, almost all the research suggesting that sugar causes inflammation is done on rats! When research has been done to try to show this inflammation in humans, it’s only showcased our livers’ incredible ability to handle fructose.

Our livers hardly convert any fructose to fat because they oxidize (burn), store, or share almost all of it (6, 7, 8, 9, 10, 11, 12, 13, 14, 15). It takes extremely large quantities of sugar, around as much as in 40 cans of soda over 2 days, for our livers to convert appreciable amounts of fructose to fat (13).

In other words, the fact that a high-fructose diet increases inflammation in rats does NOT mean that it does in humans, and it would take massive amounts of fructose to have those same inflammatory effects.

 

2. We have self-regulating sugar consumption mechanisms

One of the arguments for sugar causing inflammation is that it doesn’t satisfy us and keeps us hungry so that we eat too much of it. And that may be true, to a point. Although, eating more is certainly not a problem on its own (why “eat less and exercise more” is the worst advice for fat loss and health).

However, this argument falls short because the most important regulator of the amount of food we eat isn’t accounted for: energy.

The energy status of the liver and hypothalamus (a part of our brain) regulates the amount of food we eat (16, 17). When they don’t have enough energy, we feel hungry. And when they do have enough energy, we feel satisfied.

And guess what increases the energy of our livers and hypothalamus the most…

That’s right, sugar!

In other words, we won’t eat too much sugar as long as our bodies can use the sugar to produce energy.

 

3. Sugar’s inflammatory effects require more than just sugar

One of the many things that can inhibit energy production is polyunsaturated fats, or PUFA. But, PUFA do more than just inhibit energy production – they play a major role in inflammation.

When rats are given extremely large amounts of fructose, the JNK pathway is activated which causes inflammation. But, this pathway isn’t activated if the metabolites of PUFA are blocked, even in the presence of excessive amounts of fructose (18).

Instead, the rats appear to be the same as rats that aren’t fed excessive amounts of fructose and don’t produce large amounts of triglycerides. This suggests that the metabolites of PUFA interfere with the oxidation or storage of fructose, causing more fructose to be converted to fat.

So, the fact that rats are typically fed high-PUFA diets may also play a role in the inflammation seen when they’re given excessive amounts of fructose.

 

The Sweet Truth About Inflammation

Unless you’re eating HUGE quantities of sugar, your body can’t properly use sugar, or you’re a rat, you don’t need to worry about sugar causing inflammation.

As I mentioned in part 1, sugar (particularly fructose) has many benefits, including fueling the liver and the brain. Fructose even has anti-inflammatory and antioxidant effects (20, 21), and when given in normal amounts it actually inhibits the exact inflammatory pathways that it activates when given to rats in huge amounts (22).

But I will remind you that this doesn’t mean that all foods that have sugar are beneficial!

What it does mean is that just because a food contains sugar doesn’t mean it’s unhealthy, and we don’t have to avoid foods simply because of their sugar content.

 

References

Sugar Does NOT Cause Inflammation (Part 2)

In part 1 of this series, I explained some of the basic physiology underlying what happens when we consume sugar. I also explained why, while sugar can cause inflammation, it takes A LOT of sugar and the inflammation it causes isn’t necessarily harmful.

In this article, I’m going to explore this topic a little more in depth and explain why the research behind sugar causing inflammation is so misleading.

But before we dive into the research I’d like to first mention that I’m not going to include observational studies (association-based population studies).

There are many confounding variables in these types of studies, the biggest one being that sugar is widely considered unhealthy. So, those that consume more sugar typically care less about their health and do other unhealthy things. And the opposite is true for those who consume less sugar. (How many people do you know who try to be healthy but also drink soda every day and have doughnuts for breakfast?)

Those studies aside, there are many research studies that conclude that sugar, specifically fructose, causes inflammation. So, let’s start there.

 

Research Shows That Sugar Causes Inflammation

In chronic conditions like diabetes, heart disease, cancer, autoimmune conditions, and obesity, several markers are elevated that indicate chronic inflammation: triglycerides, free fatty acids, fasting blood glucose, fasting insulin, blood pressure, cholesterol, LDL, VLDL, TNF-a, NF-kb, IL-6, etc.

These markers are all symptoms of an inability to produce energy, which ends up causing the perpetual damage that we associate with these conditions.

For many decades, saturated fat was blamed for causing these conditions and was shown to increase these markers. But after saturated fat was vindicated, sugar (specifically fructose) took its place.

Since that point, research has been coming out showing that sugar is capable of increasing all these makers in much the same way (1).

But as we found out with saturated fat, just because something elevates those markers under certain circumstances doesn’t mean that it’s causing the chronic conditions that also show elevated levels of those markers.

And it’s more than just that.

The research showing that sugar causes inflammation can’t be extrapolated to real-world applications with human beings for 3 reasons:

  1. We’re not rats
  2. We have self-regulating sugar consumption mechanisms
  3. Sugar’s inflammatory effects require more than just sugar

Let’s break these reasons down one by one.

 

1. We’re not rats

Rats are useful model organisms because their physiology is similar to ours. But, the ability to use sugar seems to be one way that we differ significantly.

Inflammation from sugar/fructose consumption occurs when there’s too much fructose for the liver to effectively handle. At this point, the liver converts more of the fructose to triglycerides (fat) and fructose and its metabolites build up, which triggers inflammation.

For this reason, the conversion of fructose to fat in the liver is a good marker for inflammation.

But, when rats consume fructose, their livers convert many times more of it to fat than our livers do (2, 3, 4, 5).

Because sugar and fructose’s effects are dose-dependent, this difference has HUGE implications for whether sugar causes inflammation in humans! So huge, in fact, that rats are considered extremely poor models for studying fructose’s effects on the human liver (5).

But, almost all the research suggesting that sugar causes inflammation is done on rats! When research has been done to try to show this inflammation in humans, it’s only showcased our livers’ incredible ability to handle fructose.

Our livers hardly convert any fructose to fat because they oxidize (burn), store, or share almost all of it (6, 7, 8, 9, 10, 11, 12, 13, 14, 15). It takes extremely large quantities of sugar, around as much as in 40 cans of soda over 2 days, for our livers to convert appreciable amounts of fructose to fat (13).

In other words, the fact that a high-fructose diet increases inflammation in rats does NOT mean that it does in humans, and it would take massive amounts of fructose to have those same inflammatory effects.

 

2. We have self-regulating sugar consumption mechanisms

One of the arguments for sugar causing inflammation is that it doesn’t satisfy us and keeps us hungry so that we eat too much of it. And that may be true, to a point. Although, eating more is certainly not a problem on its own (why “eat less and exercise more” is the worst advice for fat loss and health).

However, this argument falls short because the most important regulator of the amount of food we eat isn’t accounted for: energy.

The energy status of the liver and hypothalamus (a part of our brain) regulates the amount of food we eat (16, 17). When they don’t have enough energy, we feel hungry. And when they do have enough energy, we feel satisfied.

And guess what increases the energy of our livers and hypothalamus the most…

That’s right, sugar!

In other words, we won’t eat too much sugar as long as our bodies can use the sugar to produce energy.

 

3. Sugar’s inflammatory effects require more than just sugar

One of the many things that can inhibit energy production is polyunsaturated fats, or PUFA. But, PUFA do more than just inhibit energy production – they play a major role in inflammation.

When rats are given extremely large amounts of fructose, the JNK pathway is activated which causes inflammation. But, this pathway isn’t activated if the metabolites of PUFA are blocked, even in the presence of excessive amounts of fructose (18).

Instead, the rats appear to be the same as rats that aren’t fed excessive amounts of fructose and don’t produce large amounts of triglycerides. This suggests that the metabolites of PUFA interfere with the oxidation or storage of fructose, causing more fructose to be converted to fat.

So, the fact that rats are typically fed high-PUFA diets may also play a role in the inflammation seen when they’re given excessive amounts of fructose.

 

The Sweet Truth About Inflammation

Unless you’re eating HUGE quantities of sugar, your body can’t properly use sugar, or you’re a rat, you don’t need to worry about sugar causing inflammation.

As I mentioned in part 1, sugar (particularly fructose) has many benefits, including fueling the liver and the brain. Fructose even has anti-inflammatory and antioxidant effects (20, 21), and when given in normal amounts it actually inhibits the exact inflammatory pathways that it activates when given to rats in huge amounts (22).

But I will remind you that this doesn’t mean that all foods that have sugar are beneficial!

What it does mean is that just because a food contains sugar doesn’t mean it’s unhealthy, and we don’t have to avoid foods simply because of their sugar content.

 

References

Sugar Does NOT Cause Inflammation (Part 2)

In part 1 of this series, I explained some of the basic physiology underlying what happens when we consume sugar. I also explained why, while sugar can cause inflammation, it takes A LOT of sugar and the inflammation it causes isn’t necessarily harmful.

In this article, I’m going to explore this topic a little more in depth and explain why the research behind sugar causing inflammation is so misleading.

But before we dive into the research I’d like to first mention that I’m not going to include observational studies (association-based population studies).

There are many confounding variables in these types of studies, the biggest one being that sugar is widely considered unhealthy. So, those that consume more sugar typically care less about their health and do other unhealthy things. And the opposite is true for those who consume less sugar. (How many people do you know who try to be healthy but also drink soda every day and have doughnuts for breakfast?)

Those studies aside, there are many research studies that conclude that sugar, specifically fructose, causes inflammation. So, let’s start there.

 

Research Shows That Sugar Causes Inflammation

In chronic conditions like diabetes, heart disease, cancer, autoimmune conditions, and obesity, several markers are elevated that indicate chronic inflammation: triglycerides, free fatty acids, fasting blood glucose, fasting insulin, blood pressure, cholesterol, LDL, VLDL, TNF-a, NF-kb, IL-6, etc.

These markers are all symptoms of an inability to produce energy, which ends up causing the perpetual damage that we associate with these conditions.

For many decades, saturated fat was blamed for causing these conditions and was shown to increase these markers. But after saturated fat was vindicated, sugar (specifically fructose) took its place.

Since that point, research has been coming out showing that sugar is capable of increasing all these makers in much the same way (1).

But as we found out with saturated fat, just because something elevates those markers under certain circumstances doesn’t mean that it’s causing the chronic conditions that also show elevated levels of those markers.

And it’s more than just that.

The research showing that sugar causes inflammation can’t be extrapolated to real-world applications with human beings for 3 reasons:

  1. We’re not rats
  2. We have self-regulating sugar consumption mechanisms
  3. Sugar’s inflammatory effects require more than just sugar

Let’s break these reasons down one by one.

 

1. We’re not rats

Rats are useful model organisms because their physiology is similar to ours. But, the ability to use sugar seems to be one way that we differ significantly.

Inflammation from sugar/fructose consumption occurs when there’s too much fructose for the liver to effectively handle. At this point, the liver converts more of the fructose to triglycerides (fat) and fructose and its metabolites build up, which triggers inflammation.

For this reason, the conversion of fructose to fat in the liver is a good marker for inflammation.

But, when rats consume fructose, their livers convert many times more of it to fat than our livers do (2, 3, 4, 5).

Because sugar and fructose’s effects are dose-dependent, this difference has HUGE implications for whether sugar causes inflammation in humans! So huge, in fact, that rats are considered extremely poor models for studying fructose’s effects on the human liver (5).

But, almost all the research suggesting that sugar causes inflammation is done on rats! When research has been done to try to show this inflammation in humans, it’s only showcased our livers’ incredible ability to handle fructose.

Our livers hardly convert any fructose to fat because they oxidize (burn), store, or share almost all of it (6, 7, 8, 9, 10, 11, 12, 13, 14, 15). It takes extremely large quantities of sugar, around as much as in 40 cans of soda over 2 days, for our livers to convert appreciable amounts of fructose to fat (13).

In other words, the fact that a high-fructose diet increases inflammation in rats does NOT mean that it does in humans, and it would take massive amounts of fructose to have those same inflammatory effects.

 

2. We have self-regulating sugar consumption mechanisms

One of the arguments for sugar causing inflammation is that it doesn’t satisfy us and keeps us hungry so that we eat too much of it. And that may be true, to a point. Although, eating more is certainly not a problem on its own (why “eat less and exercise more” is the worst advice for fat loss and health).

However, this argument falls short because the most important regulator of the amount of food we eat isn’t accounted for: energy.

The energy status of the liver and hypothalamus (a part of our brain) regulates the amount of food we eat (16, 17). When they don’t have enough energy, we feel hungry. And when they do have enough energy, we feel satisfied.

And guess what increases the energy of our livers and hypothalamus the most…

That’s right, sugar!

In other words, we won’t eat too much sugar as long as our bodies can use the sugar to produce energy.

 

3. Sugar’s inflammatory effects require more than just sugar

One of the many things that can inhibit energy production is polyunsaturated fats, or PUFA. But, PUFA do more than just inhibit energy production – they play a major role in inflammation.

When rats are given extremely large amounts of fructose, the JNK pathway is activated which causes inflammation. But, this pathway isn’t activated if the metabolites of PUFA are blocked, even in the presence of excessive amounts of fructose (18).

Instead, the rats appear to be the same as rats that aren’t fed excessive amounts of fructose and don’t produce large amounts of triglycerides. This suggests that the metabolites of PUFA interfere with the oxidation or storage of fructose, causing more fructose to be converted to fat.

So, the fact that rats are typically fed high-PUFA diets may also play a role in the inflammation seen when they’re given excessive amounts of fructose.

 

The Sweet Truth About Inflammation

Unless you’re eating HUGE quantities of sugar, your body can’t properly use sugar, or you’re a rat, you don’t need to worry about sugar causing inflammation.

As I mentioned in part 1, sugar (particularly fructose) has many benefits, including fueling the liver and the brain. Fructose even has anti-inflammatory and antioxidant effects (20, 21), and when given in normal amounts it actually inhibits the exact inflammatory pathways that it activates when given to rats in huge amounts (22).

But I will remind you that this doesn’t mean that all foods that have sugar are beneficial!

What it does mean is that just because a food contains sugar doesn’t mean it’s unhealthy, and we don’t have to avoid foods simply because of their sugar content.

 

References

Sugar Does NOT Cause Inflammation (Part 2)

In part 1 of this series, I explained some of the basic physiology underlying what happens when we consume sugar. I also explained why, while sugar can cause inflammation, it takes A LOT of sugar and the inflammation it causes isn’t necessarily harmful.

In this article, I’m going to explore this topic a little more in depth and explain why the research behind sugar causing inflammation is so misleading.

But before we dive into the research I’d like to first mention that I’m not going to include observational studies (association-based population studies).

There are many confounding variables in these types of studies, the biggest one being that sugar is widely considered unhealthy. So, those that consume more sugar typically care less about their health and do other unhealthy things. And the opposite is true for those who consume less sugar. (How many people do you know who try to be healthy but also drink soda every day and have doughnuts for breakfast?)

Those studies aside, there are many research studies that conclude that sugar, specifically fructose, causes inflammation. So, let’s start there.

 

Research Shows That Sugar Causes Inflammation

In chronic conditions like diabetes, heart disease, cancer, autoimmune conditions, and obesity, several markers are elevated that indicate chronic inflammation: triglycerides, free fatty acids, fasting blood glucose, fasting insulin, blood pressure, cholesterol, LDL, VLDL, TNF-a, NF-kb, IL-6, etc.

These markers are all symptoms of an inability to produce energy, which ends up causing the perpetual damage that we associate with these conditions.

For many decades, saturated fat was blamed for causing these conditions and was shown to increase these markers. But after saturated fat was vindicated, sugar (specifically fructose) took its place.

Since that point, research has been coming out showing that sugar is capable of increasing all these makers in much the same way (1).

But as we found out with saturated fat, just because something elevates those markers under certain circumstances doesn’t mean that it’s causing the chronic conditions that also show elevated levels of those markers.

And it’s more than just that.

The research showing that sugar causes inflammation can’t be extrapolated to real-world applications with human beings for 3 reasons:

  1. We’re not rats
  2. We have self-regulating sugar consumption mechanisms
  3. Sugar’s inflammatory effects require more than just sugar

Let’s break these reasons down one by one.

 

1. We’re not rats

Rats are useful model organisms because their physiology is similar to ours. But, the ability to use sugar seems to be one way that we differ significantly.

Inflammation from sugar/fructose consumption occurs when there’s too much fructose for the liver to effectively handle. At this point, the liver converts more of the fructose to triglycerides (fat) and fructose and its metabolites build up, which triggers inflammation.

For this reason, the conversion of fructose to fat in the liver is a good marker for inflammation.

But, when rats consume fructose, their livers convert many times more of it to fat than our livers do (2, 3, 4, 5).

Because sugar and fructose’s effects are dose-dependent, this difference has HUGE implications for whether sugar causes inflammation in humans! So huge, in fact, that rats are considered extremely poor models for studying fructose’s effects on the human liver (5).

But, almost all the research suggesting that sugar causes inflammation is done on rats! When research has been done to try to show this inflammation in humans, it’s only showcased our livers’ incredible ability to handle fructose.

Our livers hardly convert any fructose to fat because they oxidize (burn), store, or share almost all of it (6, 7, 8, 9, 10, 11, 12, 13, 14, 15). It takes extremely large quantities of sugar, around as much as in 40 cans of soda over 2 days, for our livers to convert appreciable amounts of fructose to fat (13).

In other words, the fact that a high-fructose diet increases inflammation in rats does NOT mean that it does in humans, and it would take massive amounts of fructose to have those same inflammatory effects.

 

2. We have self-regulating sugar consumption mechanisms

One of the arguments for sugar causing inflammation is that it doesn’t satisfy us and keeps us hungry so that we eat too much of it. And that may be true, to a point. Although, eating more is certainly not a problem on its own (why “eat less and exercise more” is the worst advice for fat loss and health).

However, this argument falls short because the most important regulator of the amount of food we eat isn’t accounted for: energy.

The energy status of the liver and hypothalamus (a part of our brain) regulates the amount of food we eat (16, 17). When they don’t have enough energy, we feel hungry. And when they do have enough energy, we feel satisfied.

And guess what increases the energy of our livers and hypothalamus the most…

That’s right, sugar!

In other words, we won’t eat too much sugar as long as our bodies can use the sugar to produce energy.

 

3. Sugar’s inflammatory effects require more than just sugar

One of the many things that can inhibit energy production is polyunsaturated fats, or PUFA. But, PUFA do more than just inhibit energy production – they play a major role in inflammation.

When rats are given extremely large amounts of fructose, the JNK pathway is activated which causes inflammation. But, this pathway isn’t activated if the metabolites of PUFA are blocked, even in the presence of excessive amounts of fructose (18).

Instead, the rats appear to be the same as rats that aren’t fed excessive amounts of fructose and don’t produce large amounts of triglycerides. This suggests that the metabolites of PUFA interfere with the oxidation or storage of fructose, causing more fructose to be converted to fat.

So, the fact that rats are typically fed high-PUFA diets may also play a role in the inflammation seen when they’re given excessive amounts of fructose.

 

The Sweet Truth About Inflammation

Unless you’re eating HUGE quantities of sugar, your body can’t properly use sugar, or you’re a rat, you don’t need to worry about sugar causing inflammation.

As I mentioned in part 1, sugar (particularly fructose) has many benefits, including fueling the liver and the brain. Fructose even has anti-inflammatory and antioxidant effects (20, 21), and when given in normal amounts it actually inhibits the exact inflammatory pathways that it activates when given to rats in huge amounts (22).

But I will remind you that this doesn’t mean that all foods that have sugar are beneficial!

What it does mean is that just because a food contains sugar doesn’t mean it’s unhealthy, and we don’t have to avoid foods simply because of their sugar content.

 

References

Sugar Does NOT Cause Inflammation (Part 2)

In part 1 of this series, I explained some of the basic physiology underlying what happens when we consume sugar. I also explained why, while sugar can cause inflammation, it takes A LOT of sugar and the inflammation it causes isn’t necessarily harmful.

In this article, I’m going to explore this topic a little more in depth and explain why the research behind sugar causing inflammation is so misleading.

But before we dive into the research I’d like to first mention that I’m not going to include observational studies (association-based population studies).

There are many confounding variables in these types of studies, the biggest one being that sugar is widely considered unhealthy. So, those that consume more sugar typically care less about their health and do other unhealthy things. And the opposite is true for those who consume less sugar. (How many people do you know who try to be healthy but also drink soda every day and have doughnuts for breakfast?)

Those studies aside, there are many research studies that conclude that sugar, specifically fructose, causes inflammation. So, let’s start there.

 

Research Shows That Sugar Causes Inflammation

In chronic conditions like diabetes, heart disease, cancer, autoimmune conditions, and obesity, several markers are elevated that indicate chronic inflammation: triglycerides, free fatty acids, fasting blood glucose, fasting insulin, blood pressure, cholesterol, LDL, VLDL, TNF-a, NF-kb, IL-6, etc.

These markers are all symptoms of an inability to produce energy, which ends up causing the perpetual damage that we associate with these conditions.

For many decades, saturated fat was blamed for causing these conditions and was shown to increase these markers. But after saturated fat was vindicated, sugar (specifically fructose) took its place.

Since that point, research has been coming out showing that sugar is capable of increasing all these makers in much the same way (1).

But as we found out with saturated fat, just because something elevates those markers under certain circumstances doesn’t mean that it’s causing the chronic conditions that also show elevated levels of those markers.

And it’s more than just that.

The research showing that sugar causes inflammation can’t be extrapolated to real-world applications with human beings for 3 reasons:

  1. We’re not rats
  2. We have self-regulating sugar consumption mechanisms
  3. Sugar’s inflammatory effects require more than just sugar

Let’s break these reasons down one by one.

 

1. We’re not rats

Rats are useful model organisms because their physiology is similar to ours. But, the ability to use sugar seems to be one way that we differ significantly.

Inflammation from sugar/fructose consumption occurs when there’s too much fructose for the liver to effectively handle. At this point, the liver converts more of the fructose to triglycerides (fat) and fructose and its metabolites build up, which triggers inflammation.

For this reason, the conversion of fructose to fat in the liver is a good marker for inflammation.

But, when rats consume fructose, their livers convert many times more of it to fat than our livers do (2, 3, 4, 5).

Because sugar and fructose’s effects are dose-dependent, this difference has HUGE implications for whether sugar causes inflammation in humans! So huge, in fact, that rats are considered extremely poor models for studying fructose’s effects on the human liver (5).

But, almost all the research suggesting that sugar causes inflammation is done on rats! When research has been done to try to show this inflammation in humans, it’s only showcased our livers’ incredible ability to handle fructose.

Our livers hardly convert any fructose to fat because they oxidize (burn), store, or share almost all of it (6, 7, 8, 9, 10, 11, 12, 13, 14, 15). It takes extremely large quantities of sugar, around as much as in 40 cans of soda over 2 days, for our livers to convert appreciable amounts of fructose to fat (13).

In other words, the fact that a high-fructose diet increases inflammation in rats does NOT mean that it does in humans, and it would take massive amounts of fructose to have those same inflammatory effects.

 

2. We have self-regulating sugar consumption mechanisms

One of the arguments for sugar causing inflammation is that it doesn’t satisfy us and keeps us hungry so that we eat too much of it. And that may be true, to a point. Although, eating more is certainly not a problem on its own (why “eat less and exercise more” is the worst advice for fat loss and health).

However, this argument falls short because the most important regulator of the amount of food we eat isn’t accounted for: energy.

The energy status of the liver and hypothalamus (a part of our brain) regulates the amount of food we eat (16, 17). When they don’t have enough energy, we feel hungry. And when they do have enough energy, we feel satisfied.

And guess what increases the energy of our livers and hypothalamus the most…

That’s right, sugar!

In other words, we won’t eat too much sugar as long as our bodies can use the sugar to produce energy.

 

3. Sugar’s inflammatory effects require more than just sugar

One of the many things that can inhibit energy production is polyunsaturated fats, or PUFA. But, PUFA do more than just inhibit energy production – they play a major role in inflammation.

When rats are given extremely large amounts of fructose, the JNK pathway is activated which causes inflammation. But, this pathway isn’t activated if the metabolites of PUFA are blocked, even in the presence of excessive amounts of fructose (18).

Instead, the rats appear to be the same as rats that aren’t fed excessive amounts of fructose and don’t produce large amounts of triglycerides. This suggests that the metabolites of PUFA interfere with the oxidation or storage of fructose, causing more fructose to be converted to fat.

So, the fact that rats are typically fed high-PUFA diets may also play a role in the inflammation seen when they’re given excessive amounts of fructose.

 

The Sweet Truth About Inflammation

Unless you’re eating HUGE quantities of sugar, your body can’t properly use sugar, or you’re a rat, you don’t need to worry about sugar causing inflammation.

As I mentioned in part 1, sugar (particularly fructose) has many benefits, including fueling the liver and the brain. Fructose even has anti-inflammatory and antioxidant effects (20, 21), and when given in normal amounts it actually inhibits the exact inflammatory pathways that it activates when given to rats in huge amounts (22).

But I will remind you that this doesn’t mean that all foods that have sugar are beneficial!

What it does mean is that just because a food contains sugar doesn’t mean it’s unhealthy, and we don’t have to avoid foods simply because of their sugar content.

 

References

Sugar Does NOT Cause Inflammation (Part 2)

In part 1 of this series, I explained some of the basic physiology underlying what happens when we consume sugar. I also explained why, while sugar can cause inflammation, it takes A LOT of sugar and the inflammation it causes isn’t necessarily harmful.

In this article, I’m going to explore this topic a little more in depth and explain why the research behind sugar causing inflammation is so misleading.

But before we dive into the research I’d like to first mention that I’m not going to include observational studies (association-based population studies).

There are many confounding variables in these types of studies, the biggest one being that sugar is widely considered unhealthy. So, those that consume more sugar typically care less about their health and do other unhealthy things. And the opposite is true for those who consume less sugar. (How many people do you know who try to be healthy but also drink soda every day and have doughnuts for breakfast?)

Those studies aside, there are many research studies that conclude that sugar, specifically fructose, causes inflammation. So, let’s start there.

 

Research Shows That Sugar Causes Inflammation

In chronic conditions like diabetes, heart disease, cancer, autoimmune conditions, and obesity, several markers are elevated that indicate chronic inflammation: triglycerides, free fatty acids, fasting blood glucose, fasting insulin, blood pressure, cholesterol, LDL, VLDL, TNF-a, NF-kb, IL-6, etc.

These markers are all symptoms of an inability to produce energy, which ends up causing the perpetual damage that we associate with these conditions.

For many decades, saturated fat was blamed for causing these conditions and was shown to increase these markers. But after saturated fat was vindicated, sugar (specifically fructose) took its place.

Since that point, research has been coming out showing that sugar is capable of increasing all these makers in much the same way (1).

But as we found out with saturated fat, just because something elevates those markers under certain circumstances doesn’t mean that it’s causing the chronic conditions that also show elevated levels of those markers.

And it’s more than just that.

The research showing that sugar causes inflammation can’t be extrapolated to real-world applications with human beings for 3 reasons:

  1. We’re not rats
  2. We have self-regulating sugar consumption mechanisms
  3. Sugar’s inflammatory effects require more than just sugar

Let’s break these reasons down one by one.

 

1. We’re not rats

Rats are useful model organisms because their physiology is similar to ours. But, the ability to use sugar seems to be one way that we differ significantly.

Inflammation from sugar/fructose consumption occurs when there’s too much fructose for the liver to effectively handle. At this point, the liver converts more of the fructose to triglycerides (fat) and fructose and its metabolites build up, which triggers inflammation.

For this reason, the conversion of fructose to fat in the liver is a good marker for inflammation.

But, when rats consume fructose, their livers convert many times more of it to fat than our livers do (2, 3, 4, 5).

Because sugar and fructose’s effects are dose-dependent, this difference has HUGE implications for whether sugar causes inflammation in humans! So huge, in fact, that rats are considered extremely poor models for studying fructose’s effects on the human liver (5).

But, almost all the research suggesting that sugar causes inflammation is done on rats! When research has been done to try to show this inflammation in humans, it’s only showcased our livers’ incredible ability to handle fructose.

Our livers hardly convert any fructose to fat because they oxidize (burn), store, or share almost all of it (6, 7, 8, 9, 10, 11, 12, 13, 14, 15). It takes extremely large quantities of sugar, around as much as in 40 cans of soda over 2 days, for our livers to convert appreciable amounts of fructose to fat (13).

In other words, the fact that a high-fructose diet increases inflammation in rats does NOT mean that it does in humans, and it would take massive amounts of fructose to have those same inflammatory effects.

 

2. We have self-regulating sugar consumption mechanisms

One of the arguments for sugar causing inflammation is that it doesn’t satisfy us and keeps us hungry so that we eat too much of it. And that may be true, to a point. Although, eating more is certainly not a problem on its own (why “eat less and exercise more” is the worst advice for fat loss and health).

However, this argument falls short because the most important regulator of the amount of food we eat isn’t accounted for: energy.

The energy status of the liver and hypothalamus (a part of our brain) regulates the amount of food we eat (16, 17). When they don’t have enough energy, we feel hungry. And when they do have enough energy, we feel satisfied.

And guess what increases the energy of our livers and hypothalamus the most…

That’s right, sugar!

In other words, we won’t eat too much sugar as long as our bodies can use the sugar to produce energy.

 

3. Sugar’s inflammatory effects require more than just sugar

One of the many things that can inhibit energy production is polyunsaturated fats, or PUFA. But, PUFA do more than just inhibit energy production – they play a major role in inflammation.

When rats are given extremely large amounts of fructose, the JNK pathway is activated which causes inflammation. But, this pathway isn’t activated if the metabolites of PUFA are blocked, even in the presence of excessive amounts of fructose (18).

Instead, the rats appear to be the same as rats that aren’t fed excessive amounts of fructose and don’t produce large amounts of triglycerides. This suggests that the metabolites of PUFA interfere with the oxidation or storage of fructose, causing more fructose to be converted to fat.

So, the fact that rats are typically fed high-PUFA diets may also play a role in the inflammation seen when they’re given excessive amounts of fructose.

 

The Sweet Truth About Inflammation

Unless you’re eating HUGE quantities of sugar, your body can’t properly use sugar, or you’re a rat, you don’t need to worry about sugar causing inflammation.

As I mentioned in part 1, sugar (particularly fructose) has many benefits, including fueling the liver and the brain. Fructose even has anti-inflammatory and antioxidant effects (20, 21), and when given in normal amounts it actually inhibits the exact inflammatory pathways that it activates when given to rats in huge amounts (22).

But I will remind you that this doesn’t mean that all foods that have sugar are beneficial!

What it does mean is that just because a food contains sugar doesn’t mean it’s unhealthy, and we don’t have to avoid foods simply because of their sugar content.

 

References

Sugar Does NOT Cause Inflammation (Part 2)

In part 1 of this series, I explained some of the basic physiology underlying what happens when we consume sugar. I also explained why, while sugar can cause inflammation, it takes A LOT of sugar and the inflammation it causes isn’t necessarily harmful.

In this article, I’m going to explore this topic a little more in depth and explain why the research behind sugar causing inflammation is so misleading.

But before we dive into the research I’d like to first mention that I’m not going to include observational studies (association-based population studies).

There are many confounding variables in these types of studies, the biggest one being that sugar is widely considered unhealthy. So, those that consume more sugar typically care less about their health and do other unhealthy things. And the opposite is true for those who consume less sugar. (How many people do you know who try to be healthy but also drink soda every day and have doughnuts for breakfast?)

Those studies aside, there are many research studies that conclude that sugar, specifically fructose, causes inflammation. So, let’s start there.

 

Research Shows That Sugar Causes Inflammation

In chronic conditions like diabetes, heart disease, cancer, autoimmune conditions, and obesity, several markers are elevated that indicate chronic inflammation: triglycerides, free fatty acids, fasting blood glucose, fasting insulin, blood pressure, cholesterol, LDL, VLDL, TNF-a, NF-kb, IL-6, etc.

These markers are all symptoms of an inability to produce energy, which ends up causing the perpetual damage that we associate with these conditions.

For many decades, saturated fat was blamed for causing these conditions and was shown to increase these markers. But after saturated fat was vindicated, sugar (specifically fructose) took its place.

Since that point, research has been coming out showing that sugar is capable of increasing all these makers in much the same way (1).

But as we found out with saturated fat, just because something elevates those markers under certain circumstances doesn’t mean that it’s causing the chronic conditions that also show elevated levels of those markers.

And it’s more than just that.

The research showing that sugar causes inflammation can’t be extrapolated to real-world applications with human beings for 3 reasons:

  1. We’re not rats
  2. We have self-regulating sugar consumption mechanisms
  3. Sugar’s inflammatory effects require more than just sugar

Let’s break these reasons down one by one.

 

1. We’re not rats

Rats are useful model organisms because their physiology is similar to ours. But, the ability to use sugar seems to be one way that we differ significantly.

Inflammation from sugar/fructose consumption occurs when there’s too much fructose for the liver to effectively handle. At this point, the liver converts more of the fructose to triglycerides (fat) and fructose and its metabolites build up, which triggers inflammation.

For this reason, the conversion of fructose to fat in the liver is a good marker for inflammation.

But, when rats consume fructose, their livers convert many times more of it to fat than our livers do (2, 3, 4, 5).

Because sugar and fructose’s effects are dose-dependent, this difference has HUGE implications for whether sugar causes inflammation in humans! So huge, in fact, that rats are considered extremely poor models for studying fructose’s effects on the human liver (5).

But, almost all the research suggesting that sugar causes inflammation is done on rats! When research has been done to try to show this inflammation in humans, it’s only showcased our livers’ incredible ability to handle fructose.

Our livers hardly convert any fructose to fat because they oxidize (burn), store, or share almost all of it (6, 7, 8, 9, 10, 11, 12, 13, 14, 15). It takes extremely large quantities of sugar, around as much as in 40 cans of soda over 2 days, for our livers to convert appreciable amounts of fructose to fat (13).

In other words, the fact that a high-fructose diet increases inflammation in rats does NOT mean that it does in humans, and it would take massive amounts of fructose to have those same inflammatory effects.

 

2. We have self-regulating sugar consumption mechanisms

One of the arguments for sugar causing inflammation is that it doesn’t satisfy us and keeps us hungry so that we eat too much of it. And that may be true, to a point. Although, eating more is certainly not a problem on its own (why “eat less and exercise more” is the worst advice for fat loss and health).

However, this argument falls short because the most important regulator of the amount of food we eat isn’t accounted for: energy.

The energy status of the liver and hypothalamus (a part of our brain) regulates the amount of food we eat (16, 17). When they don’t have enough energy, we feel hungry. And when they do have enough energy, we feel satisfied.

And guess what increases the energy of our livers and hypothalamus the most…

That’s right, sugar!

In other words, we won’t eat too much sugar as long as our bodies can use the sugar to produce energy.

 

3. Sugar’s inflammatory effects require more than just sugar

One of the many things that can inhibit energy production is polyunsaturated fats, or PUFA. But, PUFA do more than just inhibit energy production – they play a major role in inflammation.

When rats are given extremely large amounts of fructose, the JNK pathway is activated which causes inflammation. But, this pathway isn’t activated if the metabolites of PUFA are blocked, even in the presence of excessive amounts of fructose (18).

Instead, the rats appear to be the same as rats that aren’t fed excessive amounts of fructose and don’t produce large amounts of triglycerides. This suggests that the metabolites of PUFA interfere with the oxidation or storage of fructose, causing more fructose to be converted to fat.

So, the fact that rats are typically fed high-PUFA diets may also play a role in the inflammation seen when they’re given excessive amounts of fructose.

 

The Sweet Truth About Inflammation

Unless you’re eating HUGE quantities of sugar, your body can’t properly use sugar, or you’re a rat, you don’t need to worry about sugar causing inflammation.

As I mentioned in part 1, sugar (particularly fructose) has many benefits, including fueling the liver and the brain. Fructose even has anti-inflammatory and antioxidant effects (20, 21), and when given in normal amounts it actually inhibits the exact inflammatory pathways that it activates when given to rats in huge amounts (22).

But I will remind you that this doesn’t mean that all foods that have sugar are beneficial!

What it does mean is that just because a food contains sugar doesn’t mean it’s unhealthy, and we don’t have to avoid foods simply because of their sugar content.

 

References

Sugar Does NOT Cause Inflammation (Part 2)

In part 1 of this series, I explained some of the basic physiology underlying what happens when we consume sugar. I also explained why, while sugar can cause inflammation, it takes A LOT of sugar and the inflammation it causes isn’t necessarily harmful.

In this article, I’m going to explore this topic a little more in depth and explain why the research behind sugar causing inflammation is so misleading.

But before we dive into the research I’d like to first mention that I’m not going to include observational studies (association-based population studies).

There are many confounding variables in these types of studies, the biggest one being that sugar is widely considered unhealthy. So, those that consume more sugar typically care less about their health and do other unhealthy things. And the opposite is true for those who consume less sugar. (How many people do you know who try to be healthy but also drink soda every day and have doughnuts for breakfast?)

Those studies aside, there are many research studies that conclude that sugar, specifically fructose, causes inflammation. So, let’s start there.

 

Research Shows That Sugar Causes Inflammation

In chronic conditions like diabetes, heart disease, cancer, autoimmune conditions, and obesity, several markers are elevated that indicate chronic inflammation: triglycerides, free fatty acids, fasting blood glucose, fasting insulin, blood pressure, cholesterol, LDL, VLDL, TNF-a, NF-kb, IL-6, etc.

These markers are all symptoms of an inability to produce energy, which ends up causing the perpetual damage that we associate with these conditions.

For many decades, saturated fat was blamed for causing these conditions and was shown to increase these markers. But after saturated fat was vindicated, sugar (specifically fructose) took its place.

Since that point, research has been coming out showing that sugar is capable of increasing all these makers in much the same way (1).

But as we found out with saturated fat, just because something elevates those markers under certain circumstances doesn’t mean that it’s causing the chronic conditions that also show elevated levels of those markers.

And it’s more than just that.

The research showing that sugar causes inflammation can’t be extrapolated to real-world applications with human beings for 3 reasons:

  1. We’re not rats
  2. We have self-regulating sugar consumption mechanisms
  3. Sugar’s inflammatory effects require more than just sugar

Let’s break these reasons down one by one.

 

1. We’re not rats

Rats are useful model organisms because their physiology is similar to ours. But, the ability to use sugar seems to be one way that we differ significantly.

Inflammation from sugar/fructose consumption occurs when there’s too much fructose for the liver to effectively handle. At this point, the liver converts more of the fructose to triglycerides (fat) and fructose and its metabolites build up, which triggers inflammation.

For this reason, the conversion of fructose to fat in the liver is a good marker for inflammation.

But, when rats consume fructose, their livers convert many times more of it to fat than our livers do (2, 3, 4, 5).

Because sugar and fructose’s effects are dose-dependent, this difference has HUGE implications for whether sugar causes inflammation in humans! So huge, in fact, that rats are considered extremely poor models for studying fructose’s effects on the human liver (5).

But, almost all the research suggesting that sugar causes inflammation is done on rats! When research has been done to try to show this inflammation in humans, it’s only showcased our livers’ incredible ability to handle fructose.

Our livers hardly convert any fructose to fat because they oxidize (burn), store, or share almost all of it (6, 7, 8, 9, 10, 11, 12, 13, 14, 15). It takes extremely large quantities of sugar, around as much as in 40 cans of soda over 2 days, for our livers to convert appreciable amounts of fructose to fat (13).

In other words, the fact that a high-fructose diet increases inflammation in rats does NOT mean that it does in humans, and it would take massive amounts of fructose to have those same inflammatory effects.

 

2. We have self-regulating sugar consumption mechanisms

One of the arguments for sugar causing inflammation is that it doesn’t satisfy us and keeps us hungry so that we eat too much of it. And that may be true, to a point. Although, eating more is certainly not a problem on its own (why “eat less and exercise more” is the worst advice for fat loss and health).

However, this argument falls short because the most important regulator of the amount of food we eat isn’t accounted for: energy.

The energy status of the liver and hypothalamus (a part of our brain) regulates the amount of food we eat (16, 17). When they don’t have enough energy, we feel hungry. And when they do have enough energy, we feel satisfied.

And guess what increases the energy of our livers and hypothalamus the most…

That’s right, sugar!

In other words, we won’t eat too much sugar as long as our bodies can use the sugar to produce energy.

 

3. Sugar’s inflammatory effects require more than just sugar

One of the many things that can inhibit energy production is polyunsaturated fats, or PUFA. But, PUFA do more than just inhibit energy production – they play a major role in inflammation.

When rats are given extremely large amounts of fructose, the JNK pathway is activated which causes inflammation. But, this pathway isn’t activated if the metabolites of PUFA are blocked, even in the presence of excessive amounts of fructose (18).

Instead, the rats appear to be the same as rats that aren’t fed excessive amounts of fructose and don’t produce large amounts of triglycerides. This suggests that the metabolites of PUFA interfere with the oxidation or storage of fructose, causing more fructose to be converted to fat.

So, the fact that rats are typically fed high-PUFA diets may also play a role in the inflammation seen when they’re given excessive amounts of fructose.

 

The Sweet Truth About Inflammation

Unless you’re eating HUGE quantities of sugar, your body can’t properly use sugar, or you’re a rat, you don’t need to worry about sugar causing inflammation.

As I mentioned in part 1, sugar (particularly fructose) has many benefits, including fueling the liver and the brain. Fructose even has anti-inflammatory and antioxidant effects (20, 21), and when given in normal amounts it actually inhibits the exact inflammatory pathways that it activates when given to rats in huge amounts (22).

But I will remind you that this doesn’t mean that all foods that have sugar are beneficial!

What it does mean is that just because a food contains sugar doesn’t mean it’s unhealthy, and we don’t have to avoid foods simply because of their sugar content.

 

References

Sugar Does NOT Cause Inflammation (Part 1)

The anti-sugar agenda is stronger now than ever, and unsupported and exaggerated claims are fueling its expansion.

Sugar is blamed for everything from obesity and diabetes to heart disease and autoimmune conditions and is even considered to be “toxic” and a “poison.”

But sugar is about as far from a poison as you can get.

There are many misconceptions contributing to the demonization of sugar, one of which being that sugar causes inflammation. In the next two articles, I’m going to explain why this is not the case.

Sugar and inflammation have become inextricably linked. This inflammation is considered to be one of the most damaging effects of sugar and is believed to be at least partly responsible for sugar’s supposed role in various diseases.

But this idea is so ridiculous I don’t know where to start. It’s kind of like saying “don’t drive your car because you may drive to the hospital, and sometimes people die when they go to hospitals.” I know, it doesn’t make any sense.

Yes, people drive their cars to the hospital. And yes, people die at the hospital. But just because you drive doesn’t mean you’re going to go to the hospital, and just because people die at the hospital doesn’t mean that going to hospitals causes you to die.

In other words, eating sugar can cause inflammation. And inflammation does occur when people are unhealthy. But just because you eat sugar doesn’t mean it’s going to cause inflammation, and just because inflammation occurs when you’re unhealthy doesn’t mean that inflammation causes you to be unhealthy.

I know this all sounds a little crazy, and it is, so let me back up a bit and start by explaining what inflammation even is.

 

What is inflammation and why does it matter?

Inflammation is simply a response to damage. It acts as a signal that activates processes that stop damage from continuing.

It’s easy to think of inflammation in the context of an injury, like a cut to the skin. Once an injury like this inflicts damage, inflammation occurs which signals platelets to come and stop the bleeding.

So, inflammation is clearly not the problem, it’s just a mechanism that stops damage from continuing. But, when inflammation is chronically occurring, which happens in virtually all chronic diseases, it’s a sign that there is underlying damage that the inflammation can’t stop.

This is most common when our bodies can’t produce enough energy to handle their demands. There are a couple of reasons why this might happen:

  • We don’t have enough fuel – our bodies can’t produce energy without enough nutrients (carbs or fats, vitamins, minerals, etc.)
  • We can’t use the fuel we have – energy production can be blocked by all sorts of things, like endotoxin or polyunsaturated fats

Under these circumstances, inflammation can’t do its job of stopping the damage because the damage is a byproduct of the lack of energy, and more energy can’t be produced. This leads to the chronic inflammation that’s so often talked about as the cause of the many chronic diseases.

But, the chronic inflammation isn’t the cause of these diseases, it’s simply a byproduct of the constant damage, which is the result of a lack of energy.

So how does sugar fit into all of this?

Before we talk about that, let’s first clarify what sugar is.

 

What is Sugar?

White table sugar, or sucrose, is a carbohydrate that’s made up of 50% glucose and 50% fructose.

This is around the same ratio that’s found naturally in fruits and honey (as well as high-fructose corn syrup). In contrast, starchy carbohydrates like tubers, root vegetables, and grains contain mostly glucose with little or no fructose.

When we consume glucose, it goes to our blood and can be taken up by our entire body, including the brain, muscles, and liver.

On the other hand, when we consume fructose, the majority of it is taken up directly by the liver. This unique quality of fructose is why sugar is blamed for causing inflammation, even though this is one of fructose’s most beneficial qualities.

I know what you might be thinking: “if fructose is found in the same amount in fruit as in white table sugar, wouldn’t fruit cause inflammation too?”

While some of the hardcore anti-sugar folks do think that fruit causes inflammation, most admit that it doesn’t. But, they claim that this is only because it contains fiber, which separates it from soda, fruit juice (which is supposedly just as bad as soda), and other sugar-containing foods.

The fiber in fruit supposedly slows the absorption of fructose enough to completely abolish its toxic effects, which on the surface makes one question how toxic those effects could really be. Anyways, on to sugar and inflammation.

 

Sugar and inflammation

As I conceded in my analogy earlier, sugar can cause inflammation, which is what the anti-sugar agenda focuses on. So, let’s begin by talking about how that happens.

The liver is an extremely important and energy-intensive organ, using almost as much energy as the brain (1). It detoxifies chemicals, regulates hormones, produces digestive enzymes, and stores and releases sugar for the brain to use, among many other functions.

Fructose is our liver’s favorite fuel, which is why almost all the fructose we eat goes straight to our livers. Our livers use this fructose to produce energy, which they need a ton of to perform all their functions.

Our livers also save some of their fructose by converting it to glycogen, which is a storage form of sugar. This glycogen is extremely important because it acts as a storage form of sugar for the brain. When the brain needs more fuel, the liver breaks down the glycogen and releases it into the blood for the brain to use.

Due to the importance of storing sugar for the brain, the liver will typically store a lot of fructose in the form of glycogen – around 100 grams (this is the amount of fructose in 5 cans of soda).

But, when you feed the liver extra fructose, a couple remarkable things happen:

  • It increases the amount of fructose it burns (2).
  • It shares a large amount of the fructose with other parts of the body by releasing it as glucose and lactate, while also increasing the amount of sugar the entire body burns and stores (2, 3, 4). When this happens, the body can store as much as 1000 grams of glycogen, which is the amount of sugar in 25 cans of soda! (4) Although it should be noted that at this point you would probably have significant amounts of inflammation.

I like to think of the liver as a magic car. When you fill this car with extra gas (fructose) its engine begins to run even faster to burn the extra gas, while also sharing gas with other cars and making their engines run faster. And, the gas tank can expand to hold up to 10 times as much gas!

But, if you keep filling the car with too much gas it begins to overflow, and some of it spills out and damages the paint on the car.

This is where the inflammation comes in. If we eat so much fructose that our livers can’t burn it, share it, and store it as glycogen fast enough, it begins to overflow which causes inflammation.

But, this inflammation isn’t a bad thing! It’s a protective mechanism that stops more fuel from coming into the already-full liver.

And, this inflammation is NOT the same as the chronic inflammation seen in chronic diseases, because it’s only temporary. As the liver uses up the excess fructose (which doesn’t take long because our livers use a lot of energy), the inflammation dissipates.

 

Some concluding thoughts

Yes, sugar can cause inflammation. But, literally anything can cause inflammation depending on the dose. Water, oxygen, protein, sunlight, vitamins, minerals. This hardly constitutes the label of a “poison.”

It takes A LOT of sugar to cause inflammation. And, this isn’t the same as the chronic inflammation that goes on in chronic disease, which is due to a lack of energy.

We even have self-regulating mechanisms that stop us from consuming too much sugar. Plus, we can minimize any potential inflammatory effects of sugar by reducing PUFA consumption. (more on self-regulating sugar mechanisms and PUFA in part 2)

This is not to mention that sugar has tons of benefits. You just learned about how it fuels the liver, which is extremely important for digestion, hormone regulation, brain function, and many other processes. It also fuels the brain directly and opposes stress, as I mentioned in this article.

This isn’t to say that pure white sugar is a perfect “health food” – it’s devoid of virtually all vitamins and minerals, which can make it harmful if you’re not getting enough of these nutrients. But, it’s not the poison it’s made out to be, and just because a food contains sugar doesn’t mean that it’s unhealthy.

Fruits, fruit juice, and dried fruit, for example, are often avoided because of their sugar content. But, their sugar content is no reason to avoid them and is even a reason to eat more of them, if you ask me.

That being said, not all foods that contain sugar are healthy. Many processed foods that contain sugar also contain polyunsaturated fats and other ingredients that would most certainly exclude them from being “health foods.”

In part 2 I’ll discuss why the research behind sugar and inflammation is so misleading, as well as the role of PUFA in this inflammation and our self-regulating sugar mechanisms.

 

References

Sugar Does NOT Cause Inflammation (Part 1)

The anti-sugar agenda is stronger now than ever, and unsupported and exaggerated claims are fueling its expansion.

Sugar is blamed for everything from obesity and diabetes to heart disease and autoimmune conditions and is even considered to be “toxic” and a “poison.”

But sugar is about as far from a poison as you can get.

There are many misconceptions contributing to the demonization of sugar, one of which being that sugar causes inflammation. In the next two articles, I’m going to explain why this is not the case.

Sugar and inflammation have become inextricably linked. This inflammation is considered to be one of the most damaging effects of sugar and is believed to be at least partly responsible for sugar’s supposed role in various diseases.

But this idea is so ridiculous I don’t know where to start. It’s kind of like saying “don’t drive your car because you may drive to the hospital, and sometimes people die when they go to hospitals.” I know, it doesn’t make any sense.

Yes, people drive their cars to the hospital. And yes, people die at the hospital. But just because you drive doesn’t mean you’re going to go to the hospital, and just because people die at the hospital doesn’t mean that going to hospitals causes you to die.

In other words, eating sugar can cause inflammation. And inflammation does occur when people are unhealthy. But just because you eat sugar doesn’t mean it’s going to cause inflammation, and just because inflammation occurs when you’re unhealthy doesn’t mean that inflammation causes you to be unhealthy.

I know this all sounds a little crazy, and it is, so let me back up a bit and start by explaining what inflammation even is.

 

What is inflammation and why does it matter?

Inflammation is simply a response to damage. It acts as a signal that activates processes that stop damage from continuing.

It’s easy to think of inflammation in the context of an injury, like a cut to the skin. Once an injury like this inflicts damage, inflammation occurs which signals platelets to come and stop the bleeding.

So, inflammation is clearly not the problem, it’s just a mechanism that stops damage from continuing. But, when inflammation is chronically occurring, which happens in virtually all chronic diseases, it’s a sign that there is underlying damage that the inflammation can’t stop.

This is most common when our bodies can’t produce enough energy to handle their demands. There are a couple of reasons why this might happen:

  • We don’t have enough fuel – our bodies can’t produce energy without enough nutrients (carbs or fats, vitamins, minerals, etc.)
  • We can’t use the fuel we have – energy production can be blocked by all sorts of things, like endotoxin or polyunsaturated fats

Under these circumstances, inflammation can’t do its job of stopping the damage because the damage is a byproduct of the lack of energy, and more energy can’t be produced. This leads to the chronic inflammation that’s so often talked about as the cause of the many chronic diseases.

But, the chronic inflammation isn’t the cause of these diseases, it’s simply a byproduct of the constant damage, which is the result of a lack of energy.

So how does sugar fit into all of this?

Before we talk about that, let’s first clarify what sugar is.

 

What is Sugar?

White table sugar, or sucrose, is a carbohydrate that’s made up of 50% glucose and 50% fructose.

This is around the same ratio that’s found naturally in fruits and honey (as well as high-fructose corn syrup). In contrast, starchy carbohydrates like tubers, root vegetables, and grains contain mostly glucose with little or no fructose.

When we consume glucose, it goes to our blood and can be taken up by our entire body, including the brain, muscles, and liver.

On the other hand, when we consume fructose, the majority of it is taken up directly by the liver. This unique quality of fructose is why sugar is blamed for causing inflammation, even though this is one of fructose’s most beneficial qualities.

I know what you might be thinking: “if fructose is found in the same amount in fruit as in white table sugar, wouldn’t fruit cause inflammation too?”

While some of the hardcore anti-sugar folks do think that fruit causes inflammation, most admit that it doesn’t. But, they claim that this is only because it contains fiber, which separates it from soda, fruit juice (which is supposedly just as bad as soda), and other sugar-containing foods.

The fiber in fruit supposedly slows the absorption of fructose enough to completely abolish its toxic effects, which on the surface makes one question how toxic those effects could really be. Anyways, on to sugar and inflammation.

 

Sugar and inflammation

As I conceded in my analogy earlier, sugar can cause inflammation, which is what the anti-sugar agenda focuses on. So, let’s begin by talking about how that happens.

The liver is an extremely important and energy-intensive organ, using almost as much energy as the brain (1). It detoxifies chemicals, regulates hormones, produces digestive enzymes, and stores and releases sugar for the brain to use, among many other functions.

Fructose is our liver’s favorite fuel, which is why almost all the fructose we eat goes straight to our livers. Our livers use this fructose to produce energy, which they need a ton of to perform all their functions.

Our livers also save some of their fructose by converting it to glycogen, which is a storage form of sugar. This glycogen is extremely important because it acts as a storage form of sugar for the brain. When the brain needs more fuel, the liver breaks down the glycogen and releases it into the blood for the brain to use.

Due to the importance of storing sugar for the brain, the liver will typically store a lot of fructose in the form of glycogen – around 100 grams (this is the amount of fructose in 5 cans of soda).

But, when you feed the liver extra fructose, a couple remarkable things happen:

  • It increases the amount of fructose it burns (2).
  • It shares a large amount of the fructose with other parts of the body by releasing it as glucose and lactate, while also increasing the amount of sugar the entire body burns and stores (2, 3, 4). When this happens, the body can store as much as 1000 grams of glycogen, which is the amount of sugar in 25 cans of soda! (4) Although it should be noted that at this point you would probably have significant amounts of inflammation.

I like to think of the liver as a magic car. When you fill this car with extra gas (fructose) its engine begins to run even faster to burn the extra gas, while also sharing gas with other cars and making their engines run faster. And, the gas tank can expand to hold up to 10 times as much gas!

But, if you keep filling the car with too much gas it begins to overflow, and some of it spills out and damages the paint on the car.

This is where the inflammation comes in. If we eat so much fructose that our livers can’t burn it, share it, and store it as glycogen fast enough, it begins to overflow which causes inflammation.

But, this inflammation isn’t a bad thing! It’s a protective mechanism that stops more fuel from coming into the already-full liver.

And, this inflammation is NOT the same as the chronic inflammation seen in chronic diseases, because it’s only temporary. As the liver uses up the excess fructose (which doesn’t take long because our livers use a lot of energy), the inflammation dissipates.

 

Some concluding thoughts

Yes, sugar can cause inflammation. But, literally anything can cause inflammation depending on the dose. Water, oxygen, protein, sunlight, vitamins, minerals. This hardly constitutes the label of a “poison.”

It takes A LOT of sugar to cause inflammation. And, this isn’t the same as the chronic inflammation that goes on in chronic disease, which is due to a lack of energy.

We even have self-regulating mechanisms that stop us from consuming too much sugar. Plus, we can minimize any potential inflammatory effects of sugar by reducing PUFA consumption. (more on self-regulating sugar mechanisms and PUFA in part 2)

This is not to mention that sugar has tons of benefits. You just learned about how it fuels the liver, which is extremely important for digestion, hormone regulation, brain function, and many other processes. It also fuels the brain directly and opposes stress, as I mentioned in this article.

This isn’t to say that pure white sugar is a perfect “health food” – it’s devoid of virtually all vitamins and minerals, which can make it harmful if you’re not getting enough of these nutrients. But, it’s not the poison it’s made out to be, and just because a food contains sugar doesn’t mean that it’s unhealthy.

Fruits, fruit juice, and dried fruit, for example, are often avoided because of their sugar content. But, their sugar content is no reason to avoid them and is even a reason to eat more of them, if you ask me.

That being said, not all foods that contain sugar are healthy. Many processed foods that contain sugar also contain polyunsaturated fats and other ingredients that would most certainly exclude them from being “health foods.”

In part 2 I’ll discuss why the research behind sugar and inflammation is so misleading, as well as the role of PUFA in this inflammation and our self-regulating sugar mechanisms.

 

References

Sugar Does NOT Cause Inflammation (Part 1)

The anti-sugar agenda is stronger now than ever, and unsupported and exaggerated claims are fueling its expansion.

Sugar is blamed for everything from obesity and diabetes to heart disease and autoimmune conditions and is even considered to be “toxic” and a “poison.”

But sugar is about as far from a poison as you can get.

There are many misconceptions contributing to the demonization of sugar, one of which being that sugar causes inflammation. In the next two articles, I’m going to explain why this is not the case.

Sugar and inflammation have become inextricably linked. This inflammation is considered to be one of the most damaging effects of sugar and is believed to be at least partly responsible for sugar’s supposed role in various diseases.

But this idea is so ridiculous I don’t know where to start. It’s kind of like saying “don’t drive your car because you may drive to the hospital, and sometimes people die when they go to hospitals.” I know, it doesn’t make any sense.

Yes, people drive their cars to the hospital. And yes, people die at the hospital. But just because you drive doesn’t mean you’re going to go to the hospital, and just because people die at the hospital doesn’t mean that going to hospitals causes you to die.

In other words, eating sugar can cause inflammation. And inflammation does occur when people are unhealthy. But just because you eat sugar doesn’t mean it’s going to cause inflammation, and just because inflammation occurs when you’re unhealthy doesn’t mean that inflammation causes you to be unhealthy.

I know this all sounds a little crazy, and it is, so let me back up a bit and start by explaining what inflammation even is.

 

What is inflammation and why does it matter?

Inflammation is simply a response to damage. It acts as a signal that activates processes that stop damage from continuing.

It’s easy to think of inflammation in the context of an injury, like a cut to the skin. Once an injury like this inflicts damage, inflammation occurs which signals platelets to come and stop the bleeding.

So, inflammation is clearly not the problem, it’s just a mechanism that stops damage from continuing. But, when inflammation is chronically occurring, which happens in virtually all chronic diseases, it’s a sign that there is underlying damage that the inflammation can’t stop.

This is most common when our bodies can’t produce enough energy to handle their demands. There are a couple of reasons why this might happen:

  • We don’t have enough fuel – our bodies can’t produce energy without enough nutrients (carbs or fats, vitamins, minerals, etc.)
  • We can’t use the fuel we have – energy production can be blocked by all sorts of things, like endotoxin or polyunsaturated fats

Under these circumstances, inflammation can’t do its job of stopping the damage because the damage is a byproduct of the lack of energy, and more energy can’t be produced. This leads to the chronic inflammation that’s so often talked about as the cause of the many chronic diseases.

But, the chronic inflammation isn’t the cause of these diseases, it’s simply a byproduct of the constant damage, which is the result of a lack of energy.

So how does sugar fit into all of this?

Before we talk about that, let’s first clarify what sugar is.

 

What is Sugar?

White table sugar, or sucrose, is a carbohydrate that’s made up of 50% glucose and 50% fructose.

This is around the same ratio that’s found naturally in fruits and honey (as well as high-fructose corn syrup). In contrast, starchy carbohydrates like tubers, root vegetables, and grains contain mostly glucose with little or no fructose.

When we consume glucose, it goes to our blood and can be taken up by our entire body, including the brain, muscles, and liver.

On the other hand, when we consume fructose, the majority of it is taken up directly by the liver. This unique quality of fructose is why sugar is blamed for causing inflammation, even though this is one of fructose’s most beneficial qualities.

I know what you might be thinking: “if fructose is found in the same amount in fruit as in white table sugar, wouldn’t fruit cause inflammation too?”

While some of the hardcore anti-sugar folks do think that fruit causes inflammation, most admit that it doesn’t. But, they claim that this is only because it contains fiber, which separates it from soda, fruit juice (which is supposedly just as bad as soda), and other sugar-containing foods.

The fiber in fruit supposedly slows the absorption of fructose enough to completely abolish its toxic effects, which on the surface makes one question how toxic those effects could really be. Anyways, on to sugar and inflammation.

 

Sugar and inflammation

As I conceded in my analogy earlier, sugar can cause inflammation, which is what the anti-sugar agenda focuses on. So, let’s begin by talking about how that happens.

The liver is an extremely important and energy-intensive organ, using almost as much energy as the brain (1). It detoxifies chemicals, regulates hormones, produces digestive enzymes, and stores and releases sugar for the brain to use, among many other functions.

Fructose is our liver’s favorite fuel, which is why almost all the fructose we eat goes straight to our livers. Our livers use this fructose to produce energy, which they need a ton of to perform all their functions.

Our livers also save some of their fructose by converting it to glycogen, which is a storage form of sugar. This glycogen is extremely important because it acts as a storage form of sugar for the brain. When the brain needs more fuel, the liver breaks down the glycogen and releases it into the blood for the brain to use.

Due to the importance of storing sugar for the brain, the liver will typically store a lot of fructose in the form of glycogen – around 100 grams (this is the amount of fructose in 5 cans of soda).

But, when you feed the liver extra fructose, a couple remarkable things happen:

  • It increases the amount of fructose it burns (2).
  • It shares a large amount of the fructose with other parts of the body by releasing it as glucose and lactate, while also increasing the amount of sugar the entire body burns and stores (2, 3, 4). When this happens, the body can store as much as 1000 grams of glycogen, which is the amount of sugar in 25 cans of soda! (4) Although it should be noted that at this point you would probably have significant amounts of inflammation.

I like to think of the liver as a magic car. When you fill this car with extra gas (fructose) its engine begins to run even faster to burn the extra gas, while also sharing gas with other cars and making their engines run faster. And, the gas tank can expand to hold up to 10 times as much gas!

But, if you keep filling the car with too much gas it begins to overflow, and some of it spills out and damages the paint on the car.

This is where the inflammation comes in. If we eat so much fructose that our livers can’t burn it, share it, and store it as glycogen fast enough, it begins to overflow which causes inflammation.

But, this inflammation isn’t a bad thing! It’s a protective mechanism that stops more fuel from coming into the already-full liver.

And, this inflammation is NOT the same as the chronic inflammation seen in chronic diseases, because it’s only temporary. As the liver uses up the excess fructose (which doesn’t take long because our livers use a lot of energy), the inflammation dissipates.

 

Some concluding thoughts

Yes, sugar can cause inflammation. But, literally anything can cause inflammation depending on the dose. Water, oxygen, protein, sunlight, vitamins, minerals. This hardly constitutes the label of a “poison.”

It takes A LOT of sugar to cause inflammation. And, this isn’t the same as the chronic inflammation that goes on in chronic disease, which is due to a lack of energy.

We even have self-regulating mechanisms that stop us from consuming too much sugar. Plus, we can minimize any potential inflammatory effects of sugar by reducing PUFA consumption. (more on self-regulating sugar mechanisms and PUFA in part 2)

This is not to mention that sugar has tons of benefits. You just learned about how it fuels the liver, which is extremely important for digestion, hormone regulation, brain function, and many other processes. It also fuels the brain directly and opposes stress, as I mentioned in this article.

This isn’t to say that pure white sugar is a perfect “health food” – it’s devoid of virtually all vitamins and minerals, which can make it harmful if you’re not getting enough of these nutrients. But, it’s not the poison it’s made out to be, and just because a food contains sugar doesn’t mean that it’s unhealthy.

Fruits, fruit juice, and dried fruit, for example, are often avoided because of their sugar content. But, their sugar content is no reason to avoid them and is even a reason to eat more of them, if you ask me.

That being said, not all foods that contain sugar are healthy. Many processed foods that contain sugar also contain polyunsaturated fats and other ingredients that would most certainly exclude them from being “health foods.”

In part 2 I’ll discuss why the research behind sugar and inflammation is so misleading, as well as the role of PUFA in this inflammation and our self-regulating sugar mechanisms.

 

References

Sugar Does NOT Cause Inflammation (Part 1)

The anti-sugar agenda is stronger now than ever, and unsupported and exaggerated claims are fueling its expansion.

Sugar is blamed for everything from obesity and diabetes to heart disease and autoimmune conditions and is even considered to be “toxic” and a “poison.”

But sugar is about as far from a poison as you can get.

There are many misconceptions contributing to the demonization of sugar, one of which being that sugar causes inflammation. In the next two articles, I’m going to explain why this is not the case.

Sugar and inflammation have become inextricably linked. This inflammation is considered to be one of the most damaging effects of sugar and is believed to be at least partly responsible for sugar’s supposed role in various diseases.

But this idea is so ridiculous I don’t know where to start. It’s kind of like saying “don’t drive your car because you may drive to the hospital, and sometimes people die when they go to hospitals.” I know, it doesn’t make any sense.

Yes, people drive their cars to the hospital. And yes, people die at the hospital. But just because you drive doesn’t mean you’re going to go to the hospital, and just because people die at the hospital doesn’t mean that going to hospitals causes you to die.

In other words, eating sugar can cause inflammation. And inflammation does occur when people are unhealthy. But just because you eat sugar doesn’t mean it’s going to cause inflammation, and just because inflammation occurs when you’re unhealthy doesn’t mean that inflammation causes you to be unhealthy.

I know this all sounds a little crazy, and it is, so let me back up a bit and start by explaining what inflammation even is.

 

What is inflammation and why does it matter?

Inflammation is simply a response to damage. It acts as a signal that activates processes that stop damage from continuing.

It’s easy to think of inflammation in the context of an injury, like a cut to the skin. Once an injury like this inflicts damage, inflammation occurs which signals platelets to come and stop the bleeding.

So, inflammation is clearly not the problem, it’s just a mechanism that stops damage from continuing. But, when inflammation is chronically occurring, which happens in virtually all chronic diseases, it’s a sign that there is underlying damage that the inflammation can’t stop.

This is most common when our bodies can’t produce enough energy to handle their demands. There are a couple of reasons why this might happen:

  • We don’t have enough fuel – our bodies can’t produce energy without enough nutrients (carbs or fats, vitamins, minerals, etc.)
  • We can’t use the fuel we have – energy production can be blocked by all sorts of things, like endotoxin or polyunsaturated fats

Under these circumstances, inflammation can’t do its job of stopping the damage because the damage is a byproduct of the lack of energy, and more energy can’t be produced. This leads to the chronic inflammation that’s so often talked about as the cause of the many chronic diseases.

But, the chronic inflammation isn’t the cause of these diseases, it’s simply a byproduct of the constant damage, which is the result of a lack of energy.

So how does sugar fit into all of this?

Before we talk about that, let’s first clarify what sugar is.

 

What is Sugar?

White table sugar, or sucrose, is a carbohydrate that’s made up of 50% glucose and 50% fructose.

This is around the same ratio that’s found naturally in fruits and honey (as well as high-fructose corn syrup). In contrast, starchy carbohydrates like tubers, root vegetables, and grains contain mostly glucose with little or no fructose.

When we consume glucose, it goes to our blood and can be taken up by our entire body, including the brain, muscles, and liver.

On the other hand, when we consume fructose, the majority of it is taken up directly by the liver. This unique quality of fructose is why sugar is blamed for causing inflammation, even though this is one of fructose’s most beneficial qualities.

I know what you might be thinking: “if fructose is found in the same amount in fruit as in white table sugar, wouldn’t fruit cause inflammation too?”

While some of the hardcore anti-sugar folks do think that fruit causes inflammation, most admit that it doesn’t. But, they claim that this is only because it contains fiber, which separates it from soda, fruit juice (which is supposedly just as bad as soda), and other sugar-containing foods.

The fiber in fruit supposedly slows the absorption of fructose enough to completely abolish its toxic effects, which on the surface makes one question how toxic those effects could really be. Anyways, on to sugar and inflammation.

 

Sugar and inflammation

As I conceded in my analogy earlier, sugar can cause inflammation, which is what the anti-sugar agenda focuses on. So, let’s begin by talking about how that happens.

The liver is an extremely important and energy-intensive organ, using almost as much energy as the brain (1). It detoxifies chemicals, regulates hormones, produces digestive enzymes, and stores and releases sugar for the brain to use, among many other functions.

Fructose is our liver’s favorite fuel, which is why almost all the fructose we eat goes straight to our livers. Our livers use this fructose to produce energy, which they need a ton of to perform all their functions.

Our livers also save some of their fructose by converting it to glycogen, which is a storage form of sugar. This glycogen is extremely important because it acts as a storage form of sugar for the brain. When the brain needs more fuel, the liver breaks down the glycogen and releases it into the blood for the brain to use.

Due to the importance of storing sugar for the brain, the liver will typically store a lot of fructose in the form of glycogen – around 100 grams (this is the amount of fructose in 5 cans of soda).

But, when you feed the liver extra fructose, a couple remarkable things happen:

  • It increases the amount of fructose it burns (2).
  • It shares a large amount of the fructose with other parts of the body by releasing it as glucose and lactate, while also increasing the amount of sugar the entire body burns and stores (2, 3, 4). When this happens, the body can store as much as 1000 grams of glycogen, which is the amount of sugar in 25 cans of soda! (4) Although it should be noted that at this point you would probably have significant amounts of inflammation.

I like to think of the liver as a magic car. When you fill this car with extra gas (fructose) its engine begins to run even faster to burn the extra gas, while also sharing gas with other cars and making their engines run faster. And, the gas tank can expand to hold up to 10 times as much gas!

But, if you keep filling the car with too much gas it begins to overflow, and some of it spills out and damages the paint on the car.

This is where the inflammation comes in. If we eat so much fructose that our livers can’t burn it, share it, and store it as glycogen fast enough, it begins to overflow which causes inflammation.

But, this inflammation isn’t a bad thing! It’s a protective mechanism that stops more fuel from coming into the already-full liver.

And, this inflammation is NOT the same as the chronic inflammation seen in chronic diseases, because it’s only temporary. As the liver uses up the excess fructose (which doesn’t take long because our livers use a lot of energy), the inflammation dissipates.

 

Some concluding thoughts

Yes, sugar can cause inflammation. But, literally anything can cause inflammation depending on the dose. Water, oxygen, protein, sunlight, vitamins, minerals. This hardly constitutes the label of a “poison.”

It takes A LOT of sugar to cause inflammation. And, this isn’t the same as the chronic inflammation that goes on in chronic disease, which is due to a lack of energy.

We even have self-regulating mechanisms that stop us from consuming too much sugar. Plus, we can minimize any potential inflammatory effects of sugar by reducing PUFA consumption. (more on self-regulating sugar mechanisms and PUFA in part 2)

This is not to mention that sugar has tons of benefits. You just learned about how it fuels the liver, which is extremely important for digestion, hormone regulation, brain function, and many other processes. It also fuels the brain directly and opposes stress, as I mentioned in this article.

This isn’t to say that pure white sugar is a perfect “health food” – it’s devoid of virtually all vitamins and minerals, which can make it harmful if you’re not getting enough of these nutrients. But, it’s not the poison it’s made out to be, and just because a food contains sugar doesn’t mean that it’s unhealthy.

Fruits, fruit juice, and dried fruit, for example, are often avoided because of their sugar content. But, their sugar content is no reason to avoid them and is even a reason to eat more of them, if you ask me.

That being said, not all foods that contain sugar are healthy. Many processed foods that contain sugar also contain polyunsaturated fats and other ingredients that would most certainly exclude them from being “health foods.”

In part 2 I’ll discuss why the research behind sugar and inflammation is so misleading, as well as the role of PUFA in this inflammation and our self-regulating sugar mechanisms.

 

References

Sugar Does NOT Cause Inflammation (Part 1)

The anti-sugar agenda is stronger now than ever, and unsupported and exaggerated claims are fueling its expansion.

Sugar is blamed for everything from obesity and diabetes to heart disease and autoimmune conditions and is even considered to be “toxic” and a “poison.”

But sugar is about as far from a poison as you can get.

There are many misconceptions contributing to the demonization of sugar, one of which being that sugar causes inflammation. In the next two articles, I’m going to explain why this is not the case.

Sugar and inflammation have become inextricably linked. This inflammation is considered to be one of the most damaging effects of sugar and is believed to be at least partly responsible for sugar’s supposed role in various diseases.

But this idea is so ridiculous I don’t know where to start. It’s kind of like saying “don’t drive your car because you may drive to the hospital, and sometimes people die when they go to hospitals.” I know, it doesn’t make any sense.

Yes, people drive their cars to the hospital. And yes, people die at the hospital. But just because you drive doesn’t mean you’re going to go to the hospital, and just because people die at the hospital doesn’t mean that going to hospitals causes you to die.

In other words, eating sugar can cause inflammation. And inflammation does occur when people are unhealthy. But just because you eat sugar doesn’t mean it’s going to cause inflammation, and just because inflammation occurs when you’re unhealthy doesn’t mean that inflammation causes you to be unhealthy.

I know this all sounds a little crazy, and it is, so let me back up a bit and start by explaining what inflammation even is.

 

What is inflammation and why does it matter?

Inflammation is simply a response to damage. It acts as a signal that activates processes that stop damage from continuing.

It’s easy to think of inflammation in the context of an injury, like a cut to the skin. Once an injury like this inflicts damage, inflammation occurs which signals platelets to come and stop the bleeding.

So, inflammation is clearly not the problem, it’s just a mechanism that stops damage from continuing. But, when inflammation is chronically occurring, which happens in virtually all chronic diseases, it’s a sign that there is underlying damage that the inflammation can’t stop.

This is most common when our bodies can’t produce enough energy to handle their demands. There are a couple of reasons why this might happen:

  • We don’t have enough fuel – our bodies can’t produce energy without enough nutrients (carbs or fats, vitamins, minerals, etc.)
  • We can’t use the fuel we have – energy production can be blocked by all sorts of things, like endotoxin or polyunsaturated fats

Under these circumstances, inflammation can’t do its job of stopping the damage because the damage is a byproduct of the lack of energy, and more energy can’t be produced. This leads to the chronic inflammation that’s so often talked about as the cause of the many chronic diseases.

But, the chronic inflammation isn’t the cause of these diseases, it’s simply a byproduct of the constant damage, which is the result of a lack of energy.

So how does sugar fit into all of this?

Before we talk about that, let’s first clarify what sugar is.

 

What is Sugar?

White table sugar, or sucrose, is a carbohydrate that’s made up of 50% glucose and 50% fructose.

This is around the same ratio that’s found naturally in fruits and honey (as well as high-fructose corn syrup). In contrast, starchy carbohydrates like tubers, root vegetables, and grains contain mostly glucose with little or no fructose.

When we consume glucose, it goes to our blood and can be taken up by our entire body, including the brain, muscles, and liver.

On the other hand, when we consume fructose, the majority of it is taken up directly by the liver. This unique quality of fructose is why sugar is blamed for causing inflammation, even though this is one of fructose’s most beneficial qualities.

I know what you might be thinking: “if fructose is found in the same amount in fruit as in white table sugar, wouldn’t fruit cause inflammation too?”

While some of the hardcore anti-sugar folks do think that fruit causes inflammation, most admit that it doesn’t. But, they claim that this is only because it contains fiber, which separates it from soda, fruit juice (which is supposedly just as bad as soda), and other sugar-containing foods.

The fiber in fruit supposedly slows the absorption of fructose enough to completely abolish its toxic effects, which on the surface makes one question how toxic those effects could really be. Anyways, on to sugar and inflammation.

 

Sugar and inflammation

As I conceded in my analogy earlier, sugar can cause inflammation, which is what the anti-sugar agenda focuses on. So, let’s begin by talking about how that happens.

The liver is an extremely important and energy-intensive organ, using almost as much energy as the brain (1). It detoxifies chemicals, regulates hormones, produces digestive enzymes, and stores and releases sugar for the brain to use, among many other functions.

Fructose is our liver’s favorite fuel, which is why almost all the fructose we eat goes straight to our livers. Our livers use this fructose to produce energy, which they need a ton of to perform all their functions.

Our livers also save some of their fructose by converting it to glycogen, which is a storage form of sugar. This glycogen is extremely important because it acts as a storage form of sugar for the brain. When the brain needs more fuel, the liver breaks down the glycogen and releases it into the blood for the brain to use.

Due to the importance of storing sugar for the brain, the liver will typically store a lot of fructose in the form of glycogen – around 100 grams (this is the amount of fructose in 5 cans of soda).

But, when you feed the liver extra fructose, a couple remarkable things happen:

  • It increases the amount of fructose it burns (2).
  • It shares a large amount of the fructose with other parts of the body by releasing it as glucose and lactate, while also increasing the amount of sugar the entire body burns and stores (2, 3, 4). When this happens, the body can store as much as 1000 grams of glycogen, which is the amount of sugar in 25 cans of soda! (4) Although it should be noted that at this point you would probably have significant amounts of inflammation.

I like to think of the liver as a magic car. When you fill this car with extra gas (fructose) its engine begins to run even faster to burn the extra gas, while also sharing gas with other cars and making their engines run faster. And, the gas tank can expand to hold up to 10 times as much gas!

But, if you keep filling the car with too much gas it begins to overflow, and some of it spills out and damages the paint on the car.

This is where the inflammation comes in. If we eat so much fructose that our livers can’t burn it, share it, and store it as glycogen fast enough, it begins to overflow which causes inflammation.

But, this inflammation isn’t a bad thing! It’s a protective mechanism that stops more fuel from coming into the already-full liver.

And, this inflammation is NOT the same as the chronic inflammation seen in chronic diseases, because it’s only temporary. As the liver uses up the excess fructose (which doesn’t take long because our livers use a lot of energy), the inflammation dissipates.

 

Some concluding thoughts

Yes, sugar can cause inflammation. But, literally anything can cause inflammation depending on the dose. Water, oxygen, protein, sunlight, vitamins, minerals. This hardly constitutes the label of a “poison.”

It takes A LOT of sugar to cause inflammation. And, this isn’t the same as the chronic inflammation that goes on in chronic disease, which is due to a lack of energy.

We even have self-regulating mechanisms that stop us from consuming too much sugar. Plus, we can minimize any potential inflammatory effects of sugar by reducing PUFA consumption. (more on self-regulating sugar mechanisms and PUFA in part 2)

This is not to mention that sugar has tons of benefits. You just learned about how it fuels the liver, which is extremely important for digestion, hormone regulation, brain function, and many other processes. It also fuels the brain directly and opposes stress, as I mentioned in this article.

This isn’t to say that pure white sugar is a perfect “health food” – it’s devoid of virtually all vitamins and minerals, which can make it harmful if you’re not getting enough of these nutrients. But, it’s not the poison it’s made out to be, and just because a food contains sugar doesn’t mean that it’s unhealthy.

Fruits, fruit juice, and dried fruit, for example, are often avoided because of their sugar content. But, their sugar content is no reason to avoid them and is even a reason to eat more of them, if you ask me.

That being said, not all foods that contain sugar are healthy. Many processed foods that contain sugar also contain polyunsaturated fats and other ingredients that would most certainly exclude them from being “health foods.”

In part 2 I’ll discuss why the research behind sugar and inflammation is so misleading, as well as the role of PUFA in this inflammation and our self-regulating sugar mechanisms.

 

References

Sugar Does NOT Cause Inflammation (Part 1)

The anti-sugar agenda is stronger now than ever, and unsupported and exaggerated claims are fueling its expansion.

Sugar is blamed for everything from obesity and diabetes to heart disease and autoimmune conditions and is even considered to be “toxic” and a “poison.”

But sugar is about as far from a poison as you can get.

There are many misconceptions contributing to the demonization of sugar, one of which being that sugar causes inflammation. In the next two articles, I’m going to explain why this is not the case.

Sugar and inflammation have become inextricably linked. This inflammation is considered to be one of the most damaging effects of sugar and is believed to be at least partly responsible for sugar’s supposed role in various diseases.

But this idea is so ridiculous I don’t know where to start. It’s kind of like saying “don’t drive your car because you may drive to the hospital, and sometimes people die when they go to hospitals.” I know, it doesn’t make any sense.

Yes, people drive their cars to the hospital. And yes, people die at the hospital. But just because you drive doesn’t mean you’re going to go to the hospital, and just because people die at the hospital doesn’t mean that going to hospitals causes you to die.

In other words, eating sugar can cause inflammation. And inflammation does occur when people are unhealthy. But just because you eat sugar doesn’t mean it’s going to cause inflammation, and just because inflammation occurs when you’re unhealthy doesn’t mean that inflammation causes you to be unhealthy.

I know this all sounds a little crazy, and it is, so let me back up a bit and start by explaining what inflammation even is.

 

What is inflammation and why does it matter?

Inflammation is simply a response to damage. It acts as a signal that activates processes that stop damage from continuing.

It’s easy to think of inflammation in the context of an injury, like a cut to the skin. Once an injury like this inflicts damage, inflammation occurs which signals platelets to come and stop the bleeding.

So, inflammation is clearly not the problem, it’s just a mechanism that stops damage from continuing. But, when inflammation is chronically occurring, which happens in virtually all chronic diseases, it’s a sign that there is underlying damage that the inflammation can’t stop.

This is most common when our bodies can’t produce enough energy to handle their demands. There are a couple of reasons why this might happen:

  • We don’t have enough fuel – our bodies can’t produce energy without enough nutrients (carbs or fats, vitamins, minerals, etc.)
  • We can’t use the fuel we have – energy production can be blocked by all sorts of things, like endotoxin or polyunsaturated fats

Under these circumstances, inflammation can’t do its job of stopping the damage because the damage is a byproduct of the lack of energy, and more energy can’t be produced. This leads to the chronic inflammation that’s so often talked about as the cause of the many chronic diseases.

But, the chronic inflammation isn’t the cause of these diseases, it’s simply a byproduct of the constant damage, which is the result of a lack of energy.

So how does sugar fit into all of this?

Before we talk about that, let’s first clarify what sugar is.

 

What is Sugar?

White table sugar, or sucrose, is a carbohydrate that’s made up of 50% glucose and 50% fructose.

This is around the same ratio that’s found naturally in fruits and honey (as well as high-fructose corn syrup). In contrast, starchy carbohydrates like tubers, root vegetables, and grains contain mostly glucose with little or no fructose.

When we consume glucose, it goes to our blood and can be taken up by our entire body, including the brain, muscles, and liver.

On the other hand, when we consume fructose, the majority of it is taken up directly by the liver. This unique quality of fructose is why sugar is blamed for causing inflammation, even though this is one of fructose’s most beneficial qualities.

I know what you might be thinking: “if fructose is found in the same amount in fruit as in white table sugar, wouldn’t fruit cause inflammation too?”

While some of the hardcore anti-sugar folks do think that fruit causes inflammation, most admit that it doesn’t. But, they claim that this is only because it contains fiber, which separates it from soda, fruit juice (which is supposedly just as bad as soda), and other sugar-containing foods.

The fiber in fruit supposedly slows the absorption of fructose enough to completely abolish its toxic effects, which on the surface makes one question how toxic those effects could really be. Anyways, on to sugar and inflammation.

 

Sugar and inflammation

As I conceded in my analogy earlier, sugar can cause inflammation, which is what the anti-sugar agenda focuses on. So, let’s begin by talking about how that happens.

The liver is an extremely important and energy-intensive organ, using almost as much energy as the brain (1). It detoxifies chemicals, regulates hormones, produces digestive enzymes, and stores and releases sugar for the brain to use, among many other functions.

Fructose is our liver’s favorite fuel, which is why almost all the fructose we eat goes straight to our livers. Our livers use this fructose to produce energy, which they need a ton of to perform all their functions.

Our livers also save some of their fructose by converting it to glycogen, which is a storage form of sugar. This glycogen is extremely important because it acts as a storage form of sugar for the brain. When the brain needs more fuel, the liver breaks down the glycogen and releases it into the blood for the brain to use.

Due to the importance of storing sugar for the brain, the liver will typically store a lot of fructose in the form of glycogen – around 100 grams (this is the amount of fructose in 5 cans of soda).

But, when you feed the liver extra fructose, a couple remarkable things happen:

  • It increases the amount of fructose it burns (2).
  • It shares a large amount of the fructose with other parts of the body by releasing it as glucose and lactate, while also increasing the amount of sugar the entire body burns and stores (2, 3, 4). When this happens, the body can store as much as 1000 grams of glycogen, which is the amount of sugar in 25 cans of soda! (4) Although it should be noted that at this point you would probably have significant amounts of inflammation.

I like to think of the liver as a magic car. When you fill this car with extra gas (fructose) its engine begins to run even faster to burn the extra gas, while also sharing gas with other cars and making their engines run faster. And, the gas tank can expand to hold up to 10 times as much gas!

But, if you keep filling the car with too much gas it begins to overflow, and some of it spills out and damages the paint on the car.

This is where the inflammation comes in. If we eat so much fructose that our livers can’t burn it, share it, and store it as glycogen fast enough, it begins to overflow which causes inflammation.

But, this inflammation isn’t a bad thing! It’s a protective mechanism that stops more fuel from coming into the already-full liver.

And, this inflammation is NOT the same as the chronic inflammation seen in chronic diseases, because it’s only temporary. As the liver uses up the excess fructose (which doesn’t take long because our livers use a lot of energy), the inflammation dissipates.

 

Some concluding thoughts

Yes, sugar can cause inflammation. But, literally anything can cause inflammation depending on the dose. Water, oxygen, protein, sunlight, vitamins, minerals. This hardly constitutes the label of a “poison.”

It takes A LOT of sugar to cause inflammation. And, this isn’t the same as the chronic inflammation that goes on in chronic disease, which is due to a lack of energy.

We even have self-regulating mechanisms that stop us from consuming too much sugar. Plus, we can minimize any potential inflammatory effects of sugar by reducing PUFA consumption. (more on self-regulating sugar mechanisms and PUFA in part 2)

This is not to mention that sugar has tons of benefits. You just learned about how it fuels the liver, which is extremely important for digestion, hormone regulation, brain function, and many other processes. It also fuels the brain directly and opposes stress, as I mentioned in this article.

This isn’t to say that pure white sugar is a perfect “health food” – it’s devoid of virtually all vitamins and minerals, which can make it harmful if you’re not getting enough of these nutrients. But, it’s not the poison it’s made out to be, and just because a food contains sugar doesn’t mean that it’s unhealthy.

Fruits, fruit juice, and dried fruit, for example, are often avoided because of their sugar content. But, their sugar content is no reason to avoid them and is even a reason to eat more of them, if you ask me.

That being said, not all foods that contain sugar are healthy. Many processed foods that contain sugar also contain polyunsaturated fats and other ingredients that would most certainly exclude them from being “health foods.”

In part 2 I’ll discuss why the research behind sugar and inflammation is so misleading, as well as the role of PUFA in this inflammation and our self-regulating sugar mechanisms.

 

References

Sugar Does NOT Cause Inflammation (Part 1)

The anti-sugar agenda is stronger now than ever, and unsupported and exaggerated claims are fueling its expansion.

Sugar is blamed for everything from obesity and diabetes to heart disease and autoimmune conditions and is even considered to be “toxic” and a “poison.”

But sugar is about as far from a poison as you can get.

There are many misconceptions contributing to the demonization of sugar, one of which being that sugar causes inflammation. In the next two articles, I’m going to explain why this is not the case.

Sugar and inflammation have become inextricably linked. This inflammation is considered to be one of the most damaging effects of sugar and is believed to be at least partly responsible for sugar’s supposed role in various diseases.

But this idea is so ridiculous I don’t know where to start. It’s kind of like saying “don’t drive your car because you may drive to the hospital, and sometimes people die when they go to hospitals.” I know, it doesn’t make any sense.

Yes, people drive their cars to the hospital. And yes, people die at the hospital. But just because you drive doesn’t mean you’re going to go to the hospital, and just because people die at the hospital doesn’t mean that going to hospitals causes you to die.

In other words, eating sugar can cause inflammation. And inflammation does occur when people are unhealthy. But just because you eat sugar doesn’t mean it’s going to cause inflammation, and just because inflammation occurs when you’re unhealthy doesn’t mean that inflammation causes you to be unhealthy.

I know this all sounds a little crazy, and it is, so let me back up a bit and start by explaining what inflammation even is.

 

What is inflammation and why does it matter?

Inflammation is simply a response to damage. It acts as a signal that activates processes that stop damage from continuing.

It’s easy to think of inflammation in the context of an injury, like a cut to the skin. Once an injury like this inflicts damage, inflammation occurs which signals platelets to come and stop the bleeding.

So, inflammation is clearly not the problem, it’s just a mechanism that stops damage from continuing. But, when inflammation is chronically occurring, which happens in virtually all chronic diseases, it’s a sign that there is underlying damage that the inflammation can’t stop.

This is most common when our bodies can’t produce enough energy to handle their demands. There are a couple of reasons why this might happen:

  • We don’t have enough fuel – our bodies can’t produce energy without enough nutrients (carbs or fats, vitamins, minerals, etc.)
  • We can’t use the fuel we have – energy production can be blocked by all sorts of things, like endotoxin or polyunsaturated fats

Under these circumstances, inflammation can’t do its job of stopping the damage because the damage is a byproduct of the lack of energy, and more energy can’t be produced. This leads to the chronic inflammation that’s so often talked about as the cause of the many chronic diseases.

But, the chronic inflammation isn’t the cause of these diseases, it’s simply a byproduct of the constant damage, which is the result of a lack of energy.

So how does sugar fit into all of this?

Before we talk about that, let’s first clarify what sugar is.

 

What is Sugar?

White table sugar, or sucrose, is a carbohydrate that’s made up of 50% glucose and 50% fructose.

This is around the same ratio that’s found naturally in fruits and honey (as well as high-fructose corn syrup). In contrast, starchy carbohydrates like tubers, root vegetables, and grains contain mostly glucose with little or no fructose.

When we consume glucose, it goes to our blood and can be taken up by our entire body, including the brain, muscles, and liver.

On the other hand, when we consume fructose, the majority of it is taken up directly by the liver. This unique quality of fructose is why sugar is blamed for causing inflammation, even though this is one of fructose’s most beneficial qualities.

I know what you might be thinking: “if fructose is found in the same amount in fruit as in white table sugar, wouldn’t fruit cause inflammation too?”

While some of the hardcore anti-sugar folks do think that fruit causes inflammation, most admit that it doesn’t. But, they claim that this is only because it contains fiber, which separates it from soda, fruit juice (which is supposedly just as bad as soda), and other sugar-containing foods.

The fiber in fruit supposedly slows the absorption of fructose enough to completely abolish its toxic effects, which on the surface makes one question how toxic those effects could really be. Anyways, on to sugar and inflammation.

 

Sugar and inflammation

As I conceded in my analogy earlier, sugar can cause inflammation, which is what the anti-sugar agenda focuses on. So, let’s begin by talking about how that happens.

The liver is an extremely important and energy-intensive organ, using almost as much energy as the brain (1). It detoxifies chemicals, regulates hormones, produces digestive enzymes, and stores and releases sugar for the brain to use, among many other functions.

Fructose is our liver’s favorite fuel, which is why almost all the fructose we eat goes straight to our livers. Our livers use this fructose to produce energy, which they need a ton of to perform all their functions.

Our livers also save some of their fructose by converting it to glycogen, which is a storage form of sugar. This glycogen is extremely important because it acts as a storage form of sugar for the brain. When the brain needs more fuel, the liver breaks down the glycogen and releases it into the blood for the brain to use.

Due to the importance of storing sugar for the brain, the liver will typically store a lot of fructose in the form of glycogen – around 100 grams (this is the amount of fructose in 5 cans of soda).

But, when you feed the liver extra fructose, a couple remarkable things happen:

  • It increases the amount of fructose it burns (2).
  • It shares a large amount of the fructose with other parts of the body by releasing it as glucose and lactate, while also increasing the amount of sugar the entire body burns and stores (2, 3, 4). When this happens, the body can store as much as 1000 grams of glycogen, which is the amount of sugar in 25 cans of soda! (4) Although it should be noted that at this point you would probably have significant amounts of inflammation.

I like to think of the liver as a magic car. When you fill this car with extra gas (fructose) its engine begins to run even faster to burn the extra gas, while also sharing gas with other cars and making their engines run faster. And, the gas tank can expand to hold up to 10 times as much gas!

But, if you keep filling the car with too much gas it begins to overflow, and some of it spills out and damages the paint on the car.

This is where the inflammation comes in. If we eat so much fructose that our livers can’t burn it, share it, and store it as glycogen fast enough, it begins to overflow which causes inflammation.

But, this inflammation isn’t a bad thing! It’s a protective mechanism that stops more fuel from coming into the already-full liver.

And, this inflammation is NOT the same as the chronic inflammation seen in chronic diseases, because it’s only temporary. As the liver uses up the excess fructose (which doesn’t take long because our livers use a lot of energy), the inflammation dissipates.

 

Some concluding thoughts

Yes, sugar can cause inflammation. But, literally anything can cause inflammation depending on the dose. Water, oxygen, protein, sunlight, vitamins, minerals. This hardly constitutes the label of a “poison.”

It takes A LOT of sugar to cause inflammation. And, this isn’t the same as the chronic inflammation that goes on in chronic disease, which is due to a lack of energy.

We even have self-regulating mechanisms that stop us from consuming too much sugar. Plus, we can minimize any potential inflammatory effects of sugar by reducing PUFA consumption. (more on self-regulating sugar mechanisms and PUFA in part 2)

This is not to mention that sugar has tons of benefits. You just learned about how it fuels the liver, which is extremely important for digestion, hormone regulation, brain function, and many other processes. It also fuels the brain directly and opposes stress, as I mentioned in this article.

This isn’t to say that pure white sugar is a perfect “health food” – it’s devoid of virtually all vitamins and minerals, which can make it harmful if you’re not getting enough of these nutrients. But, it’s not the poison it’s made out to be, and just because a food contains sugar doesn’t mean that it’s unhealthy.

Fruits, fruit juice, and dried fruit, for example, are often avoided because of their sugar content. But, their sugar content is no reason to avoid them and is even a reason to eat more of them, if you ask me.

That being said, not all foods that contain sugar are healthy. Many processed foods that contain sugar also contain polyunsaturated fats and other ingredients that would most certainly exclude them from being “health foods.”

In part 2 I’ll discuss why the research behind sugar and inflammation is so misleading, as well as the role of PUFA in this inflammation and our self-regulating sugar mechanisms.

 

References

Sugar Does NOT Cause Inflammation (Part 1)

The anti-sugar agenda is stronger now than ever, and unsupported and exaggerated claims are fueling its expansion.

Sugar is blamed for everything from obesity and diabetes to heart disease and autoimmune conditions and is even considered to be “toxic” and a “poison.”

But sugar is about as far from a poison as you can get.

There are many misconceptions contributing to the demonization of sugar, one of which being that sugar causes inflammation. In the next two articles, I’m going to explain why this is not the case.

Sugar and inflammation have become inextricably linked. This inflammation is considered to be one of the most damaging effects of sugar and is believed to be at least partly responsible for sugar’s supposed role in various diseases.

But this idea is so ridiculous I don’t know where to start. It’s kind of like saying “don’t drive your car because you may drive to the hospital, and sometimes people die when they go to hospitals.” I know, it doesn’t make any sense.

Yes, people drive their cars to the hospital. And yes, people die at the hospital. But just because you drive doesn’t mean you’re going to go to the hospital, and just because people die at the hospital doesn’t mean that going to hospitals causes you to die.

In other words, eating sugar can cause inflammation. And inflammation does occur when people are unhealthy. But just because you eat sugar doesn’t mean it’s going to cause inflammation, and just because inflammation occurs when you’re unhealthy doesn’t mean that inflammation causes you to be unhealthy.

I know this all sounds a little crazy, and it is, so let me back up a bit and start by explaining what inflammation even is.

 

What is inflammation and why does it matter?

Inflammation is simply a response to damage. It acts as a signal that activates processes that stop damage from continuing.

It’s easy to think of inflammation in the context of an injury, like a cut to the skin. Once an injury like this inflicts damage, inflammation occurs which signals platelets to come and stop the bleeding.

So, inflammation is clearly not the problem, it’s just a mechanism that stops damage from continuing. But, when inflammation is chronically occurring, which happens in virtually all chronic diseases, it’s a sign that there is underlying damage that the inflammation can’t stop.

This is most common when our bodies can’t produce enough energy to handle their demands. There are a couple of reasons why this might happen:

  • We don’t have enough fuel – our bodies can’t produce energy without enough nutrients (carbs or fats, vitamins, minerals, etc.)
  • We can’t use the fuel we have – energy production can be blocked by all sorts of things, like endotoxin or polyunsaturated fats

Under these circumstances, inflammation can’t do its job of stopping the damage because the damage is a byproduct of the lack of energy, and more energy can’t be produced. This leads to the chronic inflammation that’s so often talked about as the cause of the many chronic diseases.

But, the chronic inflammation isn’t the cause of these diseases, it’s simply a byproduct of the constant damage, which is the result of a lack of energy.

So how does sugar fit into all of this?

Before we talk about that, let’s first clarify what sugar is.

 

What is Sugar?

White table sugar, or sucrose, is a carbohydrate that’s made up of 50% glucose and 50% fructose.

This is around the same ratio that’s found naturally in fruits and honey (as well as high-fructose corn syrup). In contrast, starchy carbohydrates like tubers, root vegetables, and grains contain mostly glucose with little or no fructose.

When we consume glucose, it goes to our blood and can be taken up by our entire body, including the brain, muscles, and liver.

On the other hand, when we consume fructose, the majority of it is taken up directly by the liver. This unique quality of fructose is why sugar is blamed for causing inflammation, even though this is one of fructose’s most beneficial qualities.

I know what you might be thinking: “if fructose is found in the same amount in fruit as in white table sugar, wouldn’t fruit cause inflammation too?”

While some of the hardcore anti-sugar folks do think that fruit causes inflammation, most admit that it doesn’t. But, they claim that this is only because it contains fiber, which separates it from soda, fruit juice (which is supposedly just as bad as soda), and other sugar-containing foods.

The fiber in fruit supposedly slows the absorption of fructose enough to completely abolish its toxic effects, which on the surface makes one question how toxic those effects could really be. Anyways, on to sugar and inflammation.

 

Sugar and inflammation

As I conceded in my analogy earlier, sugar can cause inflammation, which is what the anti-sugar agenda focuses on. So, let’s begin by talking about how that happens.

The liver is an extremely important and energy-intensive organ, using almost as much energy as the brain (1). It detoxifies chemicals, regulates hormones, produces digestive enzymes, and stores and releases sugar for the brain to use, among many other functions.

Fructose is our liver’s favorite fuel, which is why almost all the fructose we eat goes straight to our livers. Our livers use this fructose to produce energy, which they need a ton of to perform all their functions.

Our livers also save some of their fructose by converting it to glycogen, which is a storage form of sugar. This glycogen is extremely important because it acts as a storage form of sugar for the brain. When the brain needs more fuel, the liver breaks down the glycogen and releases it into the blood for the brain to use.

Due to the importance of storing sugar for the brain, the liver will typically store a lot of fructose in the form of glycogen – around 100 grams (this is the amount of fructose in 5 cans of soda).

But, when you feed the liver extra fructose, a couple remarkable things happen:

  • It increases the amount of fructose it burns (2).
  • It shares a large amount of the fructose with other parts of the body by releasing it as glucose and lactate, while also increasing the amount of sugar the entire body burns and stores (2, 3, 4). When this happens, the body can store as much as 1000 grams of glycogen, which is the amount of sugar in 25 cans of soda! (4) Although it should be noted that at this point you would probably have significant amounts of inflammation.

I like to think of the liver as a magic car. When you fill this car with extra gas (fructose) its engine begins to run even faster to burn the extra gas, while also sharing gas with other cars and making their engines run faster. And, the gas tank can expand to hold up to 10 times as much gas!

But, if you keep filling the car with too much gas it begins to overflow, and some of it spills out and damages the paint on the car.

This is where the inflammation comes in. If we eat so much fructose that our livers can’t burn it, share it, and store it as glycogen fast enough, it begins to overflow which causes inflammation.

But, this inflammation isn’t a bad thing! It’s a protective mechanism that stops more fuel from coming into the already-full liver.

And, this inflammation is NOT the same as the chronic inflammation seen in chronic diseases, because it’s only temporary. As the liver uses up the excess fructose (which doesn’t take long because our livers use a lot of energy), the inflammation dissipates.

 

Some concluding thoughts

Yes, sugar can cause inflammation. But, literally anything can cause inflammation depending on the dose. Water, oxygen, protein, sunlight, vitamins, minerals. This hardly constitutes the label of a “poison.”

It takes A LOT of sugar to cause inflammation. And, this isn’t the same as the chronic inflammation that goes on in chronic disease, which is due to a lack of energy.

We even have self-regulating mechanisms that stop us from consuming too much sugar. Plus, we can minimize any potential inflammatory effects of sugar by reducing PUFA consumption. (more on self-regulating sugar mechanisms and PUFA in part 2)

This is not to mention that sugar has tons of benefits. You just learned about how it fuels the liver, which is extremely important for digestion, hormone regulation, brain function, and many other processes. It also fuels the brain directly and opposes stress, as I mentioned in this article.

This isn’t to say that pure white sugar is a perfect “health food” – it’s devoid of virtually all vitamins and minerals, which can make it harmful if you’re not getting enough of these nutrients. But, it’s not the poison it’s made out to be, and just because a food contains sugar doesn’t mean that it’s unhealthy.

Fruits, fruit juice, and dried fruit, for example, are often avoided because of their sugar content. But, their sugar content is no reason to avoid them and is even a reason to eat more of them, if you ask me.

That being said, not all foods that contain sugar are healthy. Many processed foods that contain sugar also contain polyunsaturated fats and other ingredients that would most certainly exclude them from being “health foods.”

In part 2 I’ll discuss why the research behind sugar and inflammation is so misleading, as well as the role of PUFA in this inflammation and our self-regulating sugar mechanisms.

 

References

Sugar Does NOT Cause Inflammation (Part 1)

The anti-sugar agenda is stronger now than ever, and unsupported and exaggerated claims are fueling its expansion.

Sugar is blamed for everything from obesity and diabetes to heart disease and autoimmune conditions and is even considered to be “toxic” and a “poison.”

But sugar is about as far from a poison as you can get.

There are many misconceptions contributing to the demonization of sugar, one of which being that sugar causes inflammation. In the next two articles, I’m going to explain why this is not the case.

Sugar and inflammation have become inextricably linked. This inflammation is considered to be one of the most damaging effects of sugar and is believed to be at least partly responsible for sugar’s supposed role in various diseases.

But this idea is so ridiculous I don’t know where to start. It’s kind of like saying “don’t drive your car because you may drive to the hospital, and sometimes people die when they go to hospitals.” I know, it doesn’t make any sense.

Yes, people drive their cars to the hospital. And yes, people die at the hospital. But just because you drive doesn’t mean you’re going to go to the hospital, and just because people die at the hospital doesn’t mean that going to hospitals causes you to die.

In other words, eating sugar can cause inflammation. And inflammation does occur when people are unhealthy. But just because you eat sugar doesn’t mean it’s going to cause inflammation, and just because inflammation occurs when you’re unhealthy doesn’t mean that inflammation causes you to be unhealthy.

I know this all sounds a little crazy, and it is, so let me back up a bit and start by explaining what inflammation even is.

 

What is inflammation and why does it matter?

Inflammation is simply a response to damage. It acts as a signal that activates processes that stop damage from continuing.

It’s easy to think of inflammation in the context of an injury, like a cut to the skin. Once an injury like this inflicts damage, inflammation occurs which signals platelets to come and stop the bleeding.

So, inflammation is clearly not the problem, it’s just a mechanism that stops damage from continuing. But, when inflammation is chronically occurring, which happens in virtually all chronic diseases, it’s a sign that there is underlying damage that the inflammation can’t stop.

This is most common when our bodies can’t produce enough energy to handle their demands. There are a couple of reasons why this might happen:

  • We don’t have enough fuel – our bodies can’t produce energy without enough nutrients (carbs or fats, vitamins, minerals, etc.)
  • We can’t use the fuel we have – energy production can be blocked by all sorts of things, like endotoxin or polyunsaturated fats

Under these circumstances, inflammation can’t do its job of stopping the damage because the damage is a byproduct of the lack of energy, and more energy can’t be produced. This leads to the chronic inflammation that’s so often talked about as the cause of the many chronic diseases.

But, the chronic inflammation isn’t the cause of these diseases, it’s simply a byproduct of the constant damage, which is the result of a lack of energy.

So how does sugar fit into all of this?

Before we talk about that, let’s first clarify what sugar is.

 

What is Sugar?

White table sugar, or sucrose, is a carbohydrate that’s made up of 50% glucose and 50% fructose.

This is around the same ratio that’s found naturally in fruits and honey (as well as high-fructose corn syrup). In contrast, starchy carbohydrates like tubers, root vegetables, and grains contain mostly glucose with little or no fructose.

When we consume glucose, it goes to our blood and can be taken up by our entire body, including the brain, muscles, and liver.

On the other hand, when we consume fructose, the majority of it is taken up directly by the liver. This unique quality of fructose is why sugar is blamed for causing inflammation, even though this is one of fructose’s most beneficial qualities.

I know what you might be thinking: “if fructose is found in the same amount in fruit as in white table sugar, wouldn’t fruit cause inflammation too?”

While some of the hardcore anti-sugar folks do think that fruit causes inflammation, most admit that it doesn’t. But, they claim that this is only because it contains fiber, which separates it from soda, fruit juice (which is supposedly just as bad as soda), and other sugar-containing foods.

The fiber in fruit supposedly slows the absorption of fructose enough to completely abolish its toxic effects, which on the surface makes one question how toxic those effects could really be. Anyways, on to sugar and inflammation.

 

Sugar and inflammation

As I conceded in my analogy earlier, sugar can cause inflammation, which is what the anti-sugar agenda focuses on. So, let’s begin by talking about how that happens.

The liver is an extremely important and energy-intensive organ, using almost as much energy as the brain (1). It detoxifies chemicals, regulates hormones, produces digestive enzymes, and stores and releases sugar for the brain to use, among many other functions.

Fructose is our liver’s favorite fuel, which is why almost all the fructose we eat goes straight to our livers. Our livers use this fructose to produce energy, which they need a ton of to perform all their functions.

Our livers also save some of their fructose by converting it to glycogen, which is a storage form of sugar. This glycogen is extremely important because it acts as a storage form of sugar for the brain. When the brain needs more fuel, the liver breaks down the glycogen and releases it into the blood for the brain to use.

Due to the importance of storing sugar for the brain, the liver will typically store a lot of fructose in the form of glycogen – around 100 grams (this is the amount of fructose in 5 cans of soda).

But, when you feed the liver extra fructose, a couple remarkable things happen:

  • It increases the amount of fructose it burns (2).
  • It shares a large amount of the fructose with other parts of the body by releasing it as glucose and lactate, while also increasing the amount of sugar the entire body burns and stores (2, 3, 4). When this happens, the body can store as much as 1000 grams of glycogen, which is the amount of sugar in 25 cans of soda! (4) Although it should be noted that at this point you would probably have significant amounts of inflammation.

I like to think of the liver as a magic car. When you fill this car with extra gas (fructose) its engine begins to run even faster to burn the extra gas, while also sharing gas with other cars and making their engines run faster. And, the gas tank can expand to hold up to 10 times as much gas!

But, if you keep filling the car with too much gas it begins to overflow, and some of it spills out and damages the paint on the car.

This is where the inflammation comes in. If we eat so much fructose that our livers can’t burn it, share it, and store it as glycogen fast enough, it begins to overflow which causes inflammation.

But, this inflammation isn’t a bad thing! It’s a protective mechanism that stops more fuel from coming into the already-full liver.

And, this inflammation is NOT the same as the chronic inflammation seen in chronic diseases, because it’s only temporary. As the liver uses up the excess fructose (which doesn’t take long because our livers use a lot of energy), the inflammation dissipates.

 

Some concluding thoughts

Yes, sugar can cause inflammation. But, literally anything can cause inflammation depending on the dose. Water, oxygen, protein, sunlight, vitamins, minerals. This hardly constitutes the label of a “poison.”

It takes A LOT of sugar to cause inflammation. And, this isn’t the same as the chronic inflammation that goes on in chronic disease, which is due to a lack of energy.

We even have self-regulating mechanisms that stop us from consuming too much sugar. Plus, we can minimize any potential inflammatory effects of sugar by reducing PUFA consumption. (more on self-regulating sugar mechanisms and PUFA in part 2)

This is not to mention that sugar has tons of benefits. You just learned about how it fuels the liver, which is extremely important for digestion, hormone regulation, brain function, and many other processes. It also fuels the brain directly and opposes stress, as I mentioned in this article.

This isn’t to say that pure white sugar is a perfect “health food” – it’s devoid of virtually all vitamins and minerals, which can make it harmful if you’re not getting enough of these nutrients. But, it’s not the poison it’s made out to be, and just because a food contains sugar doesn’t mean that it’s unhealthy.

Fruits, fruit juice, and dried fruit, for example, are often avoided because of their sugar content. But, their sugar content is no reason to avoid them and is even a reason to eat more of them, if you ask me.

That being said, not all foods that contain sugar are healthy. Many processed foods that contain sugar also contain polyunsaturated fats and other ingredients that would most certainly exclude them from being “health foods.”

In part 2 I’ll discuss why the research behind sugar and inflammation is so misleading, as well as the role of PUFA in this inflammation and our self-regulating sugar mechanisms.

 

References

Sugar Does NOT Cause Inflammation (Part 1)

The anti-sugar agenda is stronger now than ever, and unsupported and exaggerated claims are fueling its expansion.

Sugar is blamed for everything from obesity and diabetes to heart disease and autoimmune conditions and is even considered to be “toxic” and a “poison.”

But sugar is about as far from a poison as you can get.

There are many misconceptions contributing to the demonization of sugar, one of which being that sugar causes inflammation. In the next two articles, I’m going to explain why this is not the case.

Sugar and inflammation have become inextricably linked. This inflammation is considered to be one of the most damaging effects of sugar and is believed to be at least partly responsible for sugar’s supposed role in various diseases.

But this idea is so ridiculous I don’t know where to start. It’s kind of like saying “don’t drive your car because you may drive to the hospital, and sometimes people die when they go to hospitals.” I know, it doesn’t make any sense.

Yes, people drive their cars to the hospital. And yes, people die at the hospital. But just because you drive doesn’t mean you’re going to go to the hospital, and just because people die at the hospital doesn’t mean that going to hospitals causes you to die.

In other words, eating sugar can cause inflammation. And inflammation does occur when people are unhealthy. But just because you eat sugar doesn’t mean it’s going to cause inflammation, and just because inflammation occurs when you’re unhealthy doesn’t mean that inflammation causes you to be unhealthy.

I know this all sounds a little crazy, and it is, so let me back up a bit and start by explaining what inflammation even is.

 

What is inflammation and why does it matter?

Inflammation is simply a response to damage. It acts as a signal that activates processes that stop damage from continuing.

It’s easy to think of inflammation in the context of an injury, like a cut to the skin. Once an injury like this inflicts damage, inflammation occurs which signals platelets to come and stop the bleeding.

So, inflammation is clearly not the problem, it’s just a mechanism that stops damage from continuing. But, when inflammation is chronically occurring, which happens in virtually all chronic diseases, it’s a sign that there is underlying damage that the inflammation can’t stop.

This is most common when our bodies can’t produce enough energy to handle their demands. There are a couple of reasons why this might happen:

  • We don’t have enough fuel – our bodies can’t produce energy without enough nutrients (carbs or fats, vitamins, minerals, etc.)
  • We can’t use the fuel we have – energy production can be blocked by all sorts of things, like endotoxin or polyunsaturated fats

Under these circumstances, inflammation can’t do its job of stopping the damage because the damage is a byproduct of the lack of energy, and more energy can’t be produced. This leads to the chronic inflammation that’s so often talked about as the cause of the many chronic diseases.

But, the chronic inflammation isn’t the cause of these diseases, it’s simply a byproduct of the constant damage, which is the result of a lack of energy.

So how does sugar fit into all of this?

Before we talk about that, let’s first clarify what sugar is.

 

What is Sugar?

White table sugar, or sucrose, is a carbohydrate that’s made up of 50% glucose and 50% fructose.

This is around the same ratio that’s found naturally in fruits and honey (as well as high-fructose corn syrup). In contrast, starchy carbohydrates like tubers, root vegetables, and grains contain mostly glucose with little or no fructose.

When we consume glucose, it goes to our blood and can be taken up by our entire body, including the brain, muscles, and liver.

On the other hand, when we consume fructose, the majority of it is taken up directly by the liver. This unique quality of fructose is why sugar is blamed for causing inflammation, even though this is one of fructose’s most beneficial qualities.

I know what you might be thinking: “if fructose is found in the same amount in fruit as in white table sugar, wouldn’t fruit cause inflammation too?”

While some of the hardcore anti-sugar folks do think that fruit causes inflammation, most admit that it doesn’t. But, they claim that this is only because it contains fiber, which separates it from soda, fruit juice (which is supposedly just as bad as soda), and other sugar-containing foods.

The fiber in fruit supposedly slows the absorption of fructose enough to completely abolish its toxic effects, which on the surface makes one question how toxic those effects could really be. Anyways, on to sugar and inflammation.

 

Sugar and inflammation

As I conceded in my analogy earlier, sugar can cause inflammation, which is what the anti-sugar agenda focuses on. So, let’s begin by talking about how that happens.

The liver is an extremely important and energy-intensive organ, using almost as much energy as the brain (1). It detoxifies chemicals, regulates hormones, produces digestive enzymes, and stores and releases sugar for the brain to use, among many other functions.

Fructose is our liver’s favorite fuel, which is why almost all the fructose we eat goes straight to our livers. Our livers use this fructose to produce energy, which they need a ton of to perform all their functions.

Our livers also save some of their fructose by converting it to glycogen, which is a storage form of sugar. This glycogen is extremely important because it acts as a storage form of sugar for the brain. When the brain needs more fuel, the liver breaks down the glycogen and releases it into the blood for the brain to use.

Due to the importance of storing sugar for the brain, the liver will typically store a lot of fructose in the form of glycogen – around 100 grams (this is the amount of fructose in 5 cans of soda).

But, when you feed the liver extra fructose, a couple remarkable things happen:

  • It increases the amount of fructose it burns (2).
  • It shares a large amount of the fructose with other parts of the body by releasing it as glucose and lactate, while also increasing the amount of sugar the entire body burns and stores (2, 3, 4). When this happens, the body can store as much as 1000 grams of glycogen, which is the amount of sugar in 25 cans of soda! (4) Although it should be noted that at this point you would probably have significant amounts of inflammation.

I like to think of the liver as a magic car. When you fill this car with extra gas (fructose) its engine begins to run even faster to burn the extra gas, while also sharing gas with other cars and making their engines run faster. And, the gas tank can expand to hold up to 10 times as much gas!

But, if you keep filling the car with too much gas it begins to overflow, and some of it spills out and damages the paint on the car.

This is where the inflammation comes in. If we eat so much fructose that our livers can’t burn it, share it, and store it as glycogen fast enough, it begins to overflow which causes inflammation.

But, this inflammation isn’t a bad thing! It’s a protective mechanism that stops more fuel from coming into the already-full liver.

And, this inflammation is NOT the same as the chronic inflammation seen in chronic diseases, because it’s only temporary. As the liver uses up the excess fructose (which doesn’t take long because our livers use a lot of energy), the inflammation dissipates.

 

Some concluding thoughts

Yes, sugar can cause inflammation. But, literally anything can cause inflammation depending on the dose. Water, oxygen, protein, sunlight, vitamins, minerals. This hardly constitutes the label of a “poison.”

It takes A LOT of sugar to cause inflammation. And, this isn’t the same as the chronic inflammation that goes on in chronic disease, which is due to a lack of energy.

We even have self-regulating mechanisms that stop us from consuming too much sugar. Plus, we can minimize any potential inflammatory effects of sugar by reducing PUFA consumption. (more on self-regulating sugar mechanisms and PUFA in part 2)

This is not to mention that sugar has tons of benefits. You just learned about how it fuels the liver, which is extremely important for digestion, hormone regulation, brain function, and many other processes. It also fuels the brain directly and opposes stress, as I mentioned in this article.

This isn’t to say that pure white sugar is a perfect “health food” – it’s devoid of virtually all vitamins and minerals, which can make it harmful if you’re not getting enough of these nutrients. But, it’s not the poison it’s made out to be, and just because a food contains sugar doesn’t mean that it’s unhealthy.

Fruits, fruit juice, and dried fruit, for example, are often avoided because of their sugar content. But, their sugar content is no reason to avoid them and is even a reason to eat more of them, if you ask me.

That being said, not all foods that contain sugar are healthy. Many processed foods that contain sugar also contain polyunsaturated fats and other ingredients that would most certainly exclude them from being “health foods.”

In part 2 I’ll discuss why the research behind sugar and inflammation is so misleading, as well as the role of PUFA in this inflammation and our self-regulating sugar mechanisms.

 

References

Sugar Does NOT Cause Inflammation (Part 1)

The anti-sugar agenda is stronger now than ever, and unsupported and exaggerated claims are fueling its expansion.

Sugar is blamed for everything from obesity and diabetes to heart disease and autoimmune conditions and is even considered to be “toxic” and a “poison.”

But sugar is about as far from a poison as you can get.

There are many misconceptions contributing to the demonization of sugar, one of which being that sugar causes inflammation. In the next two articles, I’m going to explain why this is not the case.

Sugar and inflammation have become inextricably linked. This inflammation is considered to be one of the most damaging effects of sugar and is believed to be at least partly responsible for sugar’s supposed role in various diseases.

But this idea is so ridiculous I don’t know where to start. It’s kind of like saying “don’t drive your car because you may drive to the hospital, and sometimes people die when they go to hospitals.” I know, it doesn’t make any sense.

Yes, people drive their cars to the hospital. And yes, people die at the hospital. But just because you drive doesn’t mean you’re going to go to the hospital, and just because people die at the hospital doesn’t mean that going to hospitals causes you to die.

In other words, eating sugar can cause inflammation. And inflammation does occur when people are unhealthy. But just because you eat sugar doesn’t mean it’s going to cause inflammation, and just because inflammation occurs when you’re unhealthy doesn’t mean that inflammation causes you to be unhealthy.

I know this all sounds a little crazy, and it is, so let me back up a bit and start by explaining what inflammation even is.

 

What is inflammation and why does it matter?

Inflammation is simply a response to damage. It acts as a signal that activates processes that stop damage from continuing.

It’s easy to think of inflammation in the context of an injury, like a cut to the skin. Once an injury like this inflicts damage, inflammation occurs which signals platelets to come and stop the bleeding.

So, inflammation is clearly not the problem, it’s just a mechanism that stops damage from continuing. But, when inflammation is chronically occurring, which happens in virtually all chronic diseases, it’s a sign that there is underlying damage that the inflammation can’t stop.

This is most common when our bodies can’t produce enough energy to handle their demands. There are a couple of reasons why this might happen:

  • We don’t have enough fuel – our bodies can’t produce energy without enough nutrients (carbs or fats, vitamins, minerals, etc.)
  • We can’t use the fuel we have – energy production can be blocked by all sorts of things, like endotoxin or polyunsaturated fats

Under these circumstances, inflammation can’t do its job of stopping the damage because the damage is a byproduct of the lack of energy, and more energy can’t be produced. This leads to the chronic inflammation that’s so often talked about as the cause of the many chronic diseases.

But, the chronic inflammation isn’t the cause of these diseases, it’s simply a byproduct of the constant damage, which is the result of a lack of energy.

So how does sugar fit into all of this?

Before we talk about that, let’s first clarify what sugar is.

 

What is Sugar?

White table sugar, or sucrose, is a carbohydrate that’s made up of 50% glucose and 50% fructose.

This is around the same ratio that’s found naturally in fruits and honey (as well as high-fructose corn syrup). In contrast, starchy carbohydrates like tubers, root vegetables, and grains contain mostly glucose with little or no fructose.

When we consume glucose, it goes to our blood and can be taken up by our entire body, including the brain, muscles, and liver.

On the other hand, when we consume fructose, the majority of it is taken up directly by the liver. This unique quality of fructose is why sugar is blamed for causing inflammation, even though this is one of fructose’s most beneficial qualities.

I know what you might be thinking: “if fructose is found in the same amount in fruit as in white table sugar, wouldn’t fruit cause inflammation too?”

While some of the hardcore anti-sugar folks do think that fruit causes inflammation, most admit that it doesn’t. But, they claim that this is only because it contains fiber, which separates it from soda, fruit juice (which is supposedly just as bad as soda), and other sugar-containing foods.

The fiber in fruit supposedly slows the absorption of fructose enough to completely abolish its toxic effects, which on the surface makes one question how toxic those effects could really be. Anyways, on to sugar and inflammation.

 

Sugar and inflammation

As I conceded in my analogy earlier, sugar can cause inflammation, which is what the anti-sugar agenda focuses on. So, let’s begin by talking about how that happens.

The liver is an extremely important and energy-intensive organ, using almost as much energy as the brain (1). It detoxifies chemicals, regulates hormones, produces digestive enzymes, and stores and releases sugar for the brain to use, among many other functions.

Fructose is our liver’s favorite fuel, which is why almost all the fructose we eat goes straight to our livers. Our livers use this fructose to produce energy, which they need a ton of to perform all their functions.

Our livers also save some of their fructose by converting it to glycogen, which is a storage form of sugar. This glycogen is extremely important because it acts as a storage form of sugar for the brain. When the brain needs more fuel, the liver breaks down the glycogen and releases it into the blood for the brain to use.

Due to the importance of storing sugar for the brain, the liver will typically store a lot of fructose in the form of glycogen – around 100 grams (this is the amount of fructose in 5 cans of soda).

But, when you feed the liver extra fructose, a couple remarkable things happen:

  • It increases the amount of fructose it burns (2).
  • It shares a large amount of the fructose with other parts of the body by releasing it as glucose and lactate, while also increasing the amount of sugar the entire body burns and stores (2, 3, 4). When this happens, the body can store as much as 1000 grams of glycogen, which is the amount of sugar in 25 cans of soda! (4) Although it should be noted that at this point you would probably have significant amounts of inflammation.

I like to think of the liver as a magic car. When you fill this car with extra gas (fructose) its engine begins to run even faster to burn the extra gas, while also sharing gas with other cars and making their engines run faster. And, the gas tank can expand to hold up to 10 times as much gas!

But, if you keep filling the car with too much gas it begins to overflow, and some of it spills out and damages the paint on the car.

This is where the inflammation comes in. If we eat so much fructose that our livers can’t burn it, share it, and store it as glycogen fast enough, it begins to overflow which causes inflammation.

But, this inflammation isn’t a bad thing! It’s a protective mechanism that stops more fuel from coming into the already-full liver.

And, this inflammation is NOT the same as the chronic inflammation seen in chronic diseases, because it’s only temporary. As the liver uses up the excess fructose (which doesn’t take long because our livers use a lot of energy), the inflammation dissipates.

 

Some concluding thoughts

Yes, sugar can cause inflammation. But, literally anything can cause inflammation depending on the dose. Water, oxygen, protein, sunlight, vitamins, minerals. This hardly constitutes the label of a “poison.”

It takes A LOT of sugar to cause inflammation. And, this isn’t the same as the chronic inflammation that goes on in chronic disease, which is due to a lack of energy.

We even have self-regulating mechanisms that stop us from consuming too much sugar. Plus, we can minimize any potential inflammatory effects of sugar by reducing PUFA consumption. (more on self-regulating sugar mechanisms and PUFA in part 2)

This is not to mention that sugar has tons of benefits. You just learned about how it fuels the liver, which is extremely important for digestion, hormone regulation, brain function, and many other processes. It also fuels the brain directly and opposes stress, as I mentioned in this article.

This isn’t to say that pure white sugar is a perfect “health food” – it’s devoid of virtually all vitamins and minerals, which can make it harmful if you’re not getting enough of these nutrients. But, it’s not the poison it’s made out to be, and just because a food contains sugar doesn’t mean that it’s unhealthy.

Fruits, fruit juice, and dried fruit, for example, are often avoided because of their sugar content. But, their sugar content is no reason to avoid them and is even a reason to eat more of them, if you ask me.

That being said, not all foods that contain sugar are healthy. Many processed foods that contain sugar also contain polyunsaturated fats and other ingredients that would most certainly exclude them from being “health foods.”

In part 2 I’ll discuss why the research behind sugar and inflammation is so misleading, as well as the role of PUFA in this inflammation and our self-regulating sugar mechanisms.

 

References

Sugar Does NOT Cause Inflammation (Part 1)

The anti-sugar agenda is stronger now than ever, and unsupported and exaggerated claims are fueling its expansion.

Sugar is blamed for everything from obesity and diabetes to heart disease and autoimmune conditions and is even considered to be “toxic” and a “poison.”

But sugar is about as far from a poison as you can get.

There are many misconceptions contributing to the demonization of sugar, one of which being that sugar causes inflammation. In the next two articles, I’m going to explain why this is not the case.

Sugar and inflammation have become inextricably linked. This inflammation is considered to be one of the most damaging effects of sugar and is believed to be at least partly responsible for sugar’s supposed role in various diseases.

But this idea is so ridiculous I don’t know where to start. It’s kind of like saying “don’t drive your car because you may drive to the hospital, and sometimes people die when they go to hospitals.” I know, it doesn’t make any sense.

Yes, people drive their cars to the hospital. And yes, people die at the hospital. But just because you drive doesn’t mean you’re going to go to the hospital, and just because people die at the hospital doesn’t mean that going to hospitals causes you to die.

In other words, eating sugar can cause inflammation. And inflammation does occur when people are unhealthy. But just because you eat sugar doesn’t mean it’s going to cause inflammation, and just because inflammation occurs when you’re unhealthy doesn’t mean that inflammation causes you to be unhealthy.

I know this all sounds a little crazy, and it is, so let me back up a bit and start by explaining what inflammation even is.

 

What is inflammation and why does it matter?

Inflammation is simply a response to damage. It acts as a signal that activates processes that stop damage from continuing.

It’s easy to think of inflammation in the context of an injury, like a cut to the skin. Once an injury like this inflicts damage, inflammation occurs which signals platelets to come and stop the bleeding.

So, inflammation is clearly not the problem, it’s just a mechanism that stops damage from continuing. But, when inflammation is chronically occurring, which happens in virtually all chronic diseases, it’s a sign that there is underlying damage that the inflammation can’t stop.

This is most common when our bodies can’t produce enough energy to handle their demands. There are a couple of reasons why this might happen:

  • We don’t have enough fuel – our bodies can’t produce energy without enough nutrients (carbs or fats, vitamins, minerals, etc.)
  • We can’t use the fuel we have – energy production can be blocked by all sorts of things, like endotoxin or polyunsaturated fats

Under these circumstances, inflammation can’t do its job of stopping the damage because the damage is a byproduct of the lack of energy, and more energy can’t be produced. This leads to the chronic inflammation that’s so often talked about as the cause of the many chronic diseases.

But, the chronic inflammation isn’t the cause of these diseases, it’s simply a byproduct of the constant damage, which is the result of a lack of energy.

So how does sugar fit into all of this?

Before we talk about that, let’s first clarify what sugar is.

 

What is Sugar?

White table sugar, or sucrose, is a carbohydrate that’s made up of 50% glucose and 50% fructose.

This is around the same ratio that’s found naturally in fruits and honey (as well as high-fructose corn syrup). In contrast, starchy carbohydrates like tubers, root vegetables, and grains contain mostly glucose with little or no fructose.

When we consume glucose, it goes to our blood and can be taken up by our entire body, including the brain, muscles, and liver.

On the other hand, when we consume fructose, the majority of it is taken up directly by the liver. This unique quality of fructose is why sugar is blamed for causing inflammation, even though this is one of fructose’s most beneficial qualities.

I know what you might be thinking: “if fructose is found in the same amount in fruit as in white table sugar, wouldn’t fruit cause inflammation too?”

While some of the hardcore anti-sugar folks do think that fruit causes inflammation, most admit that it doesn’t. But, they claim that this is only because it contains fiber, which separates it from soda, fruit juice (which is supposedly just as bad as soda), and other sugar-containing foods.

The fiber in fruit supposedly slows the absorption of fructose enough to completely abolish its toxic effects, which on the surface makes one question how toxic those effects could really be. Anyways, on to sugar and inflammation.

 

Sugar and inflammation

As I conceded in my analogy earlier, sugar can cause inflammation, which is what the anti-sugar agenda focuses on. So, let’s begin by talking about how that happens.

The liver is an extremely important and energy-intensive organ, using almost as much energy as the brain (1). It detoxifies chemicals, regulates hormones, produces digestive enzymes, and stores and releases sugar for the brain to use, among many other functions.

Fructose is our liver’s favorite fuel, which is why almost all the fructose we eat goes straight to our livers. Our livers use this fructose to produce energy, which they need a ton of to perform all their functions.

Our livers also save some of their fructose by converting it to glycogen, which is a storage form of sugar. This glycogen is extremely important because it acts as a storage form of sugar for the brain. When the brain needs more fuel, the liver breaks down the glycogen and releases it into the blood for the brain to use.

Due to the importance of storing sugar for the brain, the liver will typically store a lot of fructose in the form of glycogen – around 100 grams (this is the amount of fructose in 5 cans of soda).

But, when you feed the liver extra fructose, a couple remarkable things happen:

  • It increases the amount of fructose it burns (2).
  • It shares a large amount of the fructose with other parts of the body by releasing it as glucose and lactate, while also increasing the amount of sugar the entire body burns and stores (2, 3, 4). When this happens, the body can store as much as 1000 grams of glycogen, which is the amount of sugar in 25 cans of soda! (4) Although it should be noted that at this point you would probably have significant amounts of inflammation.

I like to think of the liver as a magic car. When you fill this car with extra gas (fructose) its engine begins to run even faster to burn the extra gas, while also sharing gas with other cars and making their engines run faster. And, the gas tank can expand to hold up to 10 times as much gas!

But, if you keep filling the car with too much gas it begins to overflow, and some of it spills out and damages the paint on the car.

This is where the inflammation comes in. If we eat so much fructose that our livers can’t burn it, share it, and store it as glycogen fast enough, it begins to overflow which causes inflammation.

But, this inflammation isn’t a bad thing! It’s a protective mechanism that stops more fuel from coming into the already-full liver.

And, this inflammation is NOT the same as the chronic inflammation seen in chronic diseases, because it’s only temporary. As the liver uses up the excess fructose (which doesn’t take long because our livers use a lot of energy), the inflammation dissipates.

 

Some concluding thoughts

Yes, sugar can cause inflammation. But, literally anything can cause inflammation depending on the dose. Water, oxygen, protein, sunlight, vitamins, minerals. This hardly constitutes the label of a “poison.”

It takes A LOT of sugar to cause inflammation. And, this isn’t the same as the chronic inflammation that goes on in chronic disease, which is due to a lack of energy.

We even have self-regulating mechanisms that stop us from consuming too much sugar. Plus, we can minimize any potential inflammatory effects of sugar by reducing PUFA consumption. (more on self-regulating sugar mechanisms and PUFA in part 2)

This is not to mention that sugar has tons of benefits. You just learned about how it fuels the liver, which is extremely important for digestion, hormone regulation, brain function, and many other processes. It also fuels the brain directly and opposes stress, as I mentioned in this article.

This isn’t to say that pure white sugar is a perfect “health food” – it’s devoid of virtually all vitamins and minerals, which can make it harmful if you’re not getting enough of these nutrients. But, it’s not the poison it’s made out to be, and just because a food contains sugar doesn’t mean that it’s unhealthy.

Fruits, fruit juice, and dried fruit, for example, are often avoided because of their sugar content. But, their sugar content is no reason to avoid them and is even a reason to eat more of them, if you ask me.

That being said, not all foods that contain sugar are healthy. Many processed foods that contain sugar also contain polyunsaturated fats and other ingredients that would most certainly exclude them from being “health foods.”

In part 2 I’ll discuss why the research behind sugar and inflammation is so misleading, as well as the role of PUFA in this inflammation and our self-regulating sugar mechanisms.

 

References

Sugar Does NOT Cause Inflammation (Part 1)

The anti-sugar agenda is stronger now than ever, and unsupported and exaggerated claims are fueling its expansion.

Sugar is blamed for everything from obesity and diabetes to heart disease and autoimmune conditions and is even considered to be “toxic” and a “poison.”

But sugar is about as far from a poison as you can get.

There are many misconceptions contributing to the demonization of sugar, one of which being that sugar causes inflammation. In the next two articles, I’m going to explain why this is not the case.

Sugar and inflammation have become inextricably linked. This inflammation is considered to be one of the most damaging effects of sugar and is believed to be at least partly responsible for sugar’s supposed role in various diseases.

But this idea is so ridiculous I don’t know where to start. It’s kind of like saying “don’t drive your car because you may drive to the hospital, and sometimes people die when they go to hospitals.” I know, it doesn’t make any sense.

Yes, people drive their cars to the hospital. And yes, people die at the hospital. But just because you drive doesn’t mean you’re going to go to the hospital, and just because people die at the hospital doesn’t mean that going to hospitals causes you to die.

In other words, eating sugar can cause inflammation. And inflammation does occur when people are unhealthy. But just because you eat sugar doesn’t mean it’s going to cause inflammation, and just because inflammation occurs when you’re unhealthy doesn’t mean that inflammation causes you to be unhealthy.

I know this all sounds a little crazy, and it is, so let me back up a bit and start by explaining what inflammation even is.

 

What is inflammation and why does it matter?

Inflammation is simply a response to damage. It acts as a signal that activates processes that stop damage from continuing.

It’s easy to think of inflammation in the context of an injury, like a cut to the skin. Once an injury like this inflicts damage, inflammation occurs which signals platelets to come and stop the bleeding.

So, inflammation is clearly not the problem, it’s just a mechanism that stops damage from continuing. But, when inflammation is chronically occurring, which happens in virtually all chronic diseases, it’s a sign that there is underlying damage that the inflammation can’t stop.

This is most common when our bodies can’t produce enough energy to handle their demands. There are a couple of reasons why this might happen:

  • We don’t have enough fuel – our bodies can’t produce energy without enough nutrients (carbs or fats, vitamins, minerals, etc.)
  • We can’t use the fuel we have – energy production can be blocked by all sorts of things, like endotoxin or polyunsaturated fats

Under these circumstances, inflammation can’t do its job of stopping the damage because the damage is a byproduct of the lack of energy, and more energy can’t be produced. This leads to the chronic inflammation that’s so often talked about as the cause of the many chronic diseases.

But, the chronic inflammation isn’t the cause of these diseases, it’s simply a byproduct of the constant damage, which is the result of a lack of energy.

So how does sugar fit into all of this?

Before we talk about that, let’s first clarify what sugar is.

 

What is Sugar?

White table sugar, or sucrose, is a carbohydrate that’s made up of 50% glucose and 50% fructose.

This is around the same ratio that’s found naturally in fruits and honey (as well as high-fructose corn syrup). In contrast, starchy carbohydrates like tubers, root vegetables, and grains contain mostly glucose with little or no fructose.

When we consume glucose, it goes to our blood and can be taken up by our entire body, including the brain, muscles, and liver.

On the other hand, when we consume fructose, the majority of it is taken up directly by the liver. This unique quality of fructose is why sugar is blamed for causing inflammation, even though this is one of fructose’s most beneficial qualities.

I know what you might be thinking: “if fructose is found in the same amount in fruit as in white table sugar, wouldn’t fruit cause inflammation too?”

While some of the hardcore anti-sugar folks do think that fruit causes inflammation, most admit that it doesn’t. But, they claim that this is only because it contains fiber, which separates it from soda, fruit juice (which is supposedly just as bad as soda), and other sugar-containing foods.

The fiber in fruit supposedly slows the absorption of fructose enough to completely abolish its toxic effects, which on the surface makes one question how toxic those effects could really be. Anyways, on to sugar and inflammation.

 

Sugar and inflammation

As I conceded in my analogy earlier, sugar can cause inflammation, which is what the anti-sugar agenda focuses on. So, let’s begin by talking about how that happens.

The liver is an extremely important and energy-intensive organ, using almost as much energy as the brain (1). It detoxifies chemicals, regulates hormones, produces digestive enzymes, and stores and releases sugar for the brain to use, among many other functions.

Fructose is our liver’s favorite fuel, which is why almost all the fructose we eat goes straight to our livers. Our livers use this fructose to produce energy, which they need a ton of to perform all their functions.

Our livers also save some of their fructose by converting it to glycogen, which is a storage form of sugar. This glycogen is extremely important because it acts as a storage form of sugar for the brain. When the brain needs more fuel, the liver breaks down the glycogen and releases it into the blood for the brain to use.

Due to the importance of storing sugar for the brain, the liver will typically store a lot of fructose in the form of glycogen – around 100 grams (this is the amount of fructose in 5 cans of soda).

But, when you feed the liver extra fructose, a couple remarkable things happen:

  • It increases the amount of fructose it burns (2).
  • It shares a large amount of the fructose with other parts of the body by releasing it as glucose and lactate, while also increasing the amount of sugar the entire body burns and stores (2, 3, 4). When this happens, the body can store as much as 1000 grams of glycogen, which is the amount of sugar in 25 cans of soda! (4) Although it should be noted that at this point you would probably have significant amounts of inflammation.

I like to think of the liver as a magic car. When you fill this car with extra gas (fructose) its engine begins to run even faster to burn the extra gas, while also sharing gas with other cars and making their engines run faster. And, the gas tank can expand to hold up to 10 times as much gas!

But, if you keep filling the car with too much gas it begins to overflow, and some of it spills out and damages the paint on the car.

This is where the inflammation comes in. If we eat so much fructose that our livers can’t burn it, share it, and store it as glycogen fast enough, it begins to overflow which causes inflammation.

But, this inflammation isn’t a bad thing! It’s a protective mechanism that stops more fuel from coming into the already-full liver.

And, this inflammation is NOT the same as the chronic inflammation seen in chronic diseases, because it’s only temporary. As the liver uses up the excess fructose (which doesn’t take long because our livers use a lot of energy), the inflammation dissipates.

 

Some concluding thoughts

Yes, sugar can cause inflammation. But, literally anything can cause inflammation depending on the dose. Water, oxygen, protein, sunlight, vitamins, minerals. This hardly constitutes the label of a “poison.”

It takes A LOT of sugar to cause inflammation. And, this isn’t the same as the chronic inflammation that goes on in chronic disease, which is due to a lack of energy.

We even have self-regulating mechanisms that stop us from consuming too much sugar. Plus, we can minimize any potential inflammatory effects of sugar by reducing PUFA consumption. (more on self-regulating sugar mechanisms and PUFA in part 2)

This is not to mention that sugar has tons of benefits. You just learned about how it fuels the liver, which is extremely important for digestion, hormone regulation, brain function, and many other processes. It also fuels the brain directly and opposes stress, as I mentioned in this article.

This isn’t to say that pure white sugar is a perfect “health food” – it’s devoid of virtually all vitamins and minerals, which can make it harmful if you’re not getting enough of these nutrients. But, it’s not the poison it’s made out to be, and just because a food contains sugar doesn’t mean that it’s unhealthy.

Fruits, fruit juice, and dried fruit, for example, are often avoided because of their sugar content. But, their sugar content is no reason to avoid them and is even a reason to eat more of them, if you ask me.

That being said, not all foods that contain sugar are healthy. Many processed foods that contain sugar also contain polyunsaturated fats and other ingredients that would most certainly exclude them from being “health foods.”

In part 2 I’ll discuss why the research behind sugar and inflammation is so misleading, as well as the role of PUFA in this inflammation and our self-regulating sugar mechanisms.

 

References

Sugar Does NOT Cause Inflammation (Part 1)

The anti-sugar agenda is stronger now than ever, and unsupported and exaggerated claims are fueling its expansion.

Sugar is blamed for everything from obesity and diabetes to heart disease and autoimmune conditions and is even considered to be “toxic” and a “poison.”

But sugar is about as far from a poison as you can get.

There are many misconceptions contributing to the demonization of sugar, one of which being that sugar causes inflammation. In the next two articles, I’m going to explain why this is not the case.

Sugar and inflammation have become inextricably linked. This inflammation is considered to be one of the most damaging effects of sugar and is believed to be at least partly responsible for sugar’s supposed role in various diseases.

But this idea is so ridiculous I don’t know where to start. It’s kind of like saying “don’t drive your car because you may drive to the hospital, and sometimes people die when they go to hospitals.” I know, it doesn’t make any sense.

Yes, people drive their cars to the hospital. And yes, people die at the hospital. But just because you drive doesn’t mean you’re going to go to the hospital, and just because people die at the hospital doesn’t mean that going to hospitals causes you to die.

In other words, eating sugar can cause inflammation. And inflammation does occur when people are unhealthy. But just because you eat sugar doesn’t mean it’s going to cause inflammation, and just because inflammation occurs when you’re unhealthy doesn’t mean that inflammation causes you to be unhealthy.

I know this all sounds a little crazy, and it is, so let me back up a bit and start by explaining what inflammation even is.

 

What is inflammation and why does it matter?

Inflammation is simply a response to damage. It acts as a signal that activates processes that stop damage from continuing.

It’s easy to think of inflammation in the context of an injury, like a cut to the skin. Once an injury like this inflicts damage, inflammation occurs which signals platelets to come and stop the bleeding.

So, inflammation is clearly not the problem, it’s just a mechanism that stops damage from continuing. But, when inflammation is chronically occurring, which happens in virtually all chronic diseases, it’s a sign that there is underlying damage that the inflammation can’t stop.

This is most common when our bodies can’t produce enough energy to handle their demands. There are a couple of reasons why this might happen:

  • We don’t have enough fuel – our bodies can’t produce energy without enough nutrients (carbs or fats, vitamins, minerals, etc.)
  • We can’t use the fuel we have – energy production can be blocked by all sorts of things, like endotoxin or polyunsaturated fats

Under these circumstances, inflammation can’t do its job of stopping the damage because the damage is a byproduct of the lack of energy, and more energy can’t be produced. This leads to the chronic inflammation that’s so often talked about as the cause of the many chronic diseases.

But, the chronic inflammation isn’t the cause of these diseases, it’s simply a byproduct of the constant damage, which is the result of a lack of energy.

So how does sugar fit into all of this?

Before we talk about that, let’s first clarify what sugar is.

 

What is Sugar?

White table sugar, or sucrose, is a carbohydrate that’s made up of 50% glucose and 50% fructose.

This is around the same ratio that’s found naturally in fruits and honey (as well as high-fructose corn syrup). In contrast, starchy carbohydrates like tubers, root vegetables, and grains contain mostly glucose with little or no fructose.

When we consume glucose, it goes to our blood and can be taken up by our entire body, including the brain, muscles, and liver.

On the other hand, when we consume fructose, the majority of it is taken up directly by the liver. This unique quality of fructose is why sugar is blamed for causing inflammation, even though this is one of fructose’s most beneficial qualities.

I know what you might be thinking: “if fructose is found in the same amount in fruit as in white table sugar, wouldn’t fruit cause inflammation too?”

While some of the hardcore anti-sugar folks do think that fruit causes inflammation, most admit that it doesn’t. But, they claim that this is only because it contains fiber, which separates it from soda, fruit juice (which is supposedly just as bad as soda), and other sugar-containing foods.

The fiber in fruit supposedly slows the absorption of fructose enough to completely abolish its toxic effects, which on the surface makes one question how toxic those effects could really be. Anyways, on to sugar and inflammation.

 

Sugar and inflammation

As I conceded in my analogy earlier, sugar can cause inflammation, which is what the anti-sugar agenda focuses on. So, let’s begin by talking about how that happens.

The liver is an extremely important and energy-intensive organ, using almost as much energy as the brain (1). It detoxifies chemicals, regulates hormones, produces digestive enzymes, and stores and releases sugar for the brain to use, among many other functions.

Fructose is our liver’s favorite fuel, which is why almost all the fructose we eat goes straight to our livers. Our livers use this fructose to produce energy, which they need a ton of to perform all their functions.

Our livers also save some of their fructose by converting it to glycogen, which is a storage form of sugar. This glycogen is extremely important because it acts as a storage form of sugar for the brain. When the brain needs more fuel, the liver breaks down the glycogen and releases it into the blood for the brain to use.

Due to the importance of storing sugar for the brain, the liver will typically store a lot of fructose in the form of glycogen – around 100 grams (this is the amount of fructose in 5 cans of soda).

But, when you feed the liver extra fructose, a couple remarkable things happen:

  • It increases the amount of fructose it burns (2).
  • It shares a large amount of the fructose with other parts of the body by releasing it as glucose and lactate, while also increasing the amount of sugar the entire body burns and stores (2, 3, 4). When this happens, the body can store as much as 1000 grams of glycogen, which is the amount of sugar in 25 cans of soda! (4) Although it should be noted that at this point you would probably have significant amounts of inflammation.

I like to think of the liver as a magic car. When you fill this car with extra gas (fructose) its engine begins to run even faster to burn the extra gas, while also sharing gas with other cars and making their engines run faster. And, the gas tank can expand to hold up to 10 times as much gas!

But, if you keep filling the car with too much gas it begins to overflow, and some of it spills out and damages the paint on the car.

This is where the inflammation comes in. If we eat so much fructose that our livers can’t burn it, share it, and store it as glycogen fast enough, it begins to overflow which causes inflammation.

But, this inflammation isn’t a bad thing! It’s a protective mechanism that stops more fuel from coming into the already-full liver.

And, this inflammation is NOT the same as the chronic inflammation seen in chronic diseases, because it’s only temporary. As the liver uses up the excess fructose (which doesn’t take long because our livers use a lot of energy), the inflammation dissipates.

 

Some concluding thoughts

Yes, sugar can cause inflammation. But, literally anything can cause inflammation depending on the dose. Water, oxygen, protein, sunlight, vitamins, minerals. This hardly constitutes the label of a “poison.”

It takes A LOT of sugar to cause inflammation. And, this isn’t the same as the chronic inflammation that goes on in chronic disease, which is due to a lack of energy.

We even have self-regulating mechanisms that stop us from consuming too much sugar. Plus, we can minimize any potential inflammatory effects of sugar by reducing PUFA consumption. (more on self-regulating sugar mechanisms and PUFA in part 2)

This is not to mention that sugar has tons of benefits. You just learned about how it fuels the liver, which is extremely important for digestion, hormone regulation, brain function, and many other processes. It also fuels the brain directly and opposes stress, as I mentioned in this article.

This isn’t to say that pure white sugar is a perfect “health food” – it’s devoid of virtually all vitamins and minerals, which can make it harmful if you’re not getting enough of these nutrients. But, it’s not the poison it’s made out to be, and just because a food contains sugar doesn’t mean that it’s unhealthy.

Fruits, fruit juice, and dried fruit, for example, are often avoided because of their sugar content. But, their sugar content is no reason to avoid them and is even a reason to eat more of them, if you ask me.

That being said, not all foods that contain sugar are healthy. Many processed foods that contain sugar also contain polyunsaturated fats and other ingredients that would most certainly exclude them from being “health foods.”

In part 2 I’ll discuss why the research behind sugar and inflammation is so misleading, as well as the role of PUFA in this inflammation and our self-regulating sugar mechanisms.

 

References

Sugar Does NOT Cause Inflammation (Part 1)

The anti-sugar agenda is stronger now than ever, and unsupported and exaggerated claims are fueling its expansion.

Sugar is blamed for everything from obesity and diabetes to heart disease and autoimmune conditions and is even considered to be “toxic” and a “poison.”

But sugar is about as far from a poison as you can get.

There are many misconceptions contributing to the demonization of sugar, one of which being that sugar causes inflammation. In the next two articles, I’m going to explain why this is not the case.

Sugar and inflammation have become inextricably linked. This inflammation is considered to be one of the most damaging effects of sugar and is believed to be at least partly responsible for sugar’s supposed role in various diseases.

But this idea is so ridiculous I don’t know where to start. It’s kind of like saying “don’t drive your car because you may drive to the hospital, and sometimes people die when they go to hospitals.” I know, it doesn’t make any sense.

Yes, people drive their cars to the hospital. And yes, people die at the hospital. But just because you drive doesn’t mean you’re going to go to the hospital, and just because people die at the hospital doesn’t mean that going to hospitals causes you to die.

In other words, eating sugar can cause inflammation. And inflammation does occur when people are unhealthy. But just because you eat sugar doesn’t mean it’s going to cause inflammation, and just because inflammation occurs when you’re unhealthy doesn’t mean that inflammation causes you to be unhealthy.

I know this all sounds a little crazy, and it is, so let me back up a bit and start by explaining what inflammation even is.

 

What is inflammation and why does it matter?

Inflammation is simply a response to damage. It acts as a signal that activates processes that stop damage from continuing.

It’s easy to think of inflammation in the context of an injury, like a cut to the skin. Once an injury like this inflicts damage, inflammation occurs which signals platelets to come and stop the bleeding.

So, inflammation is clearly not the problem, it’s just a mechanism that stops damage from continuing. But, when inflammation is chronically occurring, which happens in virtually all chronic diseases, it’s a sign that there is underlying damage that the inflammation can’t stop.

This is most common when our bodies can’t produce enough energy to handle their demands. There are a couple of reasons why this might happen:

  • We don’t have enough fuel – our bodies can’t produce energy without enough nutrients (carbs or fats, vitamins, minerals, etc.)
  • We can’t use the fuel we have – energy production can be blocked by all sorts of things, like endotoxin or polyunsaturated fats

Under these circumstances, inflammation can’t do its job of stopping the damage because the damage is a byproduct of the lack of energy, and more energy can’t be produced. This leads to the chronic inflammation that’s so often talked about as the cause of the many chronic diseases.

But, the chronic inflammation isn’t the cause of these diseases, it’s simply a byproduct of the constant damage, which is the result of a lack of energy.

So how does sugar fit into all of this?

Before we talk about that, let’s first clarify what sugar is.

 

What is Sugar?

White table sugar, or sucrose, is a carbohydrate that’s made up of 50% glucose and 50% fructose.

This is around the same ratio that’s found naturally in fruits and honey (as well as high-fructose corn syrup). In contrast, starchy carbohydrates like tubers, root vegetables, and grains contain mostly glucose with little or no fructose.

When we consume glucose, it goes to our blood and can be taken up by our entire body, including the brain, muscles, and liver.

On the other hand, when we consume fructose, the majority of it is taken up directly by the liver. This unique quality of fructose is why sugar is blamed for causing inflammation, even though this is one of fructose’s most beneficial qualities.

I know what you might be thinking: “if fructose is found in the same amount in fruit as in white table sugar, wouldn’t fruit cause inflammation too?”

While some of the hardcore anti-sugar folks do think that fruit causes inflammation, most admit that it doesn’t. But, they claim that this is only because it contains fiber, which separates it from soda, fruit juice (which is supposedly just as bad as soda), and other sugar-containing foods.

The fiber in fruit supposedly slows the absorption of fructose enough to completely abolish its toxic effects, which on the surface makes one question how toxic those effects could really be. Anyways, on to sugar and inflammation.

 

Sugar and inflammation

As I conceded in my analogy earlier, sugar can cause inflammation, which is what the anti-sugar agenda focuses on. So, let’s begin by talking about how that happens.

The liver is an extremely important and energy-intensive organ, using almost as much energy as the brain (1). It detoxifies chemicals, regulates hormones, produces digestive enzymes, and stores and releases sugar for the brain to use, among many other functions.

Fructose is our liver’s favorite fuel, which is why almost all the fructose we eat goes straight to our livers. Our livers use this fructose to produce energy, which they need a ton of to perform all their functions.

Our livers also save some of their fructose by converting it to glycogen, which is a storage form of sugar. This glycogen is extremely important because it acts as a storage form of sugar for the brain. When the brain needs more fuel, the liver breaks down the glycogen and releases it into the blood for the brain to use.

Due to the importance of storing sugar for the brain, the liver will typically store a lot of fructose in the form of glycogen – around 100 grams (this is the amount of fructose in 5 cans of soda).

But, when you feed the liver extra fructose, a couple remarkable things happen:

  • It increases the amount of fructose it burns (2).
  • It shares a large amount of the fructose with other parts of the body by releasing it as glucose and lactate, while also increasing the amount of sugar the entire body burns and stores (2, 3, 4). When this happens, the body can store as much as 1000 grams of glycogen, which is the amount of sugar in 25 cans of soda! (4) Although it should be noted that at this point you would probably have significant amounts of inflammation.

I like to think of the liver as a magic car. When you fill this car with extra gas (fructose) its engine begins to run even faster to burn the extra gas, while also sharing gas with other cars and making their engines run faster. And, the gas tank can expand to hold up to 10 times as much gas!

But, if you keep filling the car with too much gas it begins to overflow, and some of it spills out and damages the paint on the car.

This is where the inflammation comes in. If we eat so much fructose that our livers can’t burn it, share it, and store it as glycogen fast enough, it begins to overflow which causes inflammation.

But, this inflammation isn’t a bad thing! It’s a protective mechanism that stops more fuel from coming into the already-full liver.

And, this inflammation is NOT the same as the chronic inflammation seen in chronic diseases, because it’s only temporary. As the liver uses up the excess fructose (which doesn’t take long because our livers use a lot of energy), the inflammation dissipates.

 

Some concluding thoughts

Yes, sugar can cause inflammation. But, literally anything can cause inflammation depending on the dose. Water, oxygen, protein, sunlight, vitamins, minerals. This hardly constitutes the label of a “poison.”

It takes A LOT of sugar to cause inflammation. And, this isn’t the same as the chronic inflammation that goes on in chronic disease, which is due to a lack of energy.

We even have self-regulating mechanisms that stop us from consuming too much sugar. Plus, we can minimize any potential inflammatory effects of sugar by reducing PUFA consumption. (more on self-regulating sugar mechanisms and PUFA in part 2)

This is not to mention that sugar has tons of benefits. You just learned about how it fuels the liver, which is extremely important for digestion, hormone regulation, brain function, and many other processes. It also fuels the brain directly and opposes stress, as I mentioned in this article.

This isn’t to say that pure white sugar is a perfect “health food” – it’s devoid of virtually all vitamins and minerals, which can make it harmful if you’re not getting enough of these nutrients. But, it’s not the poison it’s made out to be, and just because a food contains sugar doesn’t mean that it’s unhealthy.

Fruits, fruit juice, and dried fruit, for example, are often avoided because of their sugar content. But, their sugar content is no reason to avoid them and is even a reason to eat more of them, if you ask me.

That being said, not all foods that contain sugar are healthy. Many processed foods that contain sugar also contain polyunsaturated fats and other ingredients that would most certainly exclude them from being “health foods.”

In part 2 I’ll discuss why the research behind sugar and inflammation is so misleading, as well as the role of PUFA in this inflammation and our self-regulating sugar mechanisms.

 

References

Sugar Does NOT Cause Inflammation (Part 1)

The anti-sugar agenda is stronger now than ever, and unsupported and exaggerated claims are fueling its expansion.

Sugar is blamed for everything from obesity and diabetes to heart disease and autoimmune conditions and is even considered to be “toxic” and a “poison.”

But sugar is about as far from a poison as you can get.

There are many misconceptions contributing to the demonization of sugar, one of which being that sugar causes inflammation. In the next two articles, I’m going to explain why this is not the case.

Sugar and inflammation have become inextricably linked. This inflammation is considered to be one of the most damaging effects of sugar and is believed to be at least partly responsible for sugar’s supposed role in various diseases.

But this idea is so ridiculous I don’t know where to start. It’s kind of like saying “don’t drive your car because you may drive to the hospital, and sometimes people die when they go to hospitals.” I know, it doesn’t make any sense.

Yes, people drive their cars to the hospital. And yes, people die at the hospital. But just because you drive doesn’t mean you’re going to go to the hospital, and just because people die at the hospital doesn’t mean that going to hospitals causes you to die.

In other words, eating sugar can cause inflammation. And inflammation does occur when people are unhealthy. But just because you eat sugar doesn’t mean it’s going to cause inflammation, and just because inflammation occurs when you’re unhealthy doesn’t mean that inflammation causes you to be unhealthy.

I know this all sounds a little crazy, and it is, so let me back up a bit and start by explaining what inflammation even is.

 

What is inflammation and why does it matter?

Inflammation is simply a response to damage. It acts as a signal that activates processes that stop damage from continuing.

It’s easy to think of inflammation in the context of an injury, like a cut to the skin. Once an injury like this inflicts damage, inflammation occurs which signals platelets to come and stop the bleeding.

So, inflammation is clearly not the problem, it’s just a mechanism that stops damage from continuing. But, when inflammation is chronically occurring, which happens in virtually all chronic diseases, it’s a sign that there is underlying damage that the inflammation can’t stop.

This is most common when our bodies can’t produce enough energy to handle their demands. There are a couple of reasons why this might happen:

  • We don’t have enough fuel – our bodies can’t produce energy without enough nutrients (carbs or fats, vitamins, minerals, etc.)
  • We can’t use the fuel we have – energy production can be blocked by all sorts of things, like endotoxin or polyunsaturated fats

Under these circumstances, inflammation can’t do its job of stopping the damage because the damage is a byproduct of the lack of energy, and more energy can’t be produced. This leads to the chronic inflammation that’s so often talked about as the cause of the many chronic diseases.

But, the chronic inflammation isn’t the cause of these diseases, it’s simply a byproduct of the constant damage, which is the result of a lack of energy.

So how does sugar fit into all of this?

Before we talk about that, let’s first clarify what sugar is.

 

What is Sugar?

White table sugar, or sucrose, is a carbohydrate that’s made up of 50% glucose and 50% fructose.

This is around the same ratio that’s found naturally in fruits and honey (as well as high-fructose corn syrup). In contrast, starchy carbohydrates like tubers, root vegetables, and grains contain mostly glucose with little or no fructose.

When we consume glucose, it goes to our blood and can be taken up by our entire body, including the brain, muscles, and liver.

On the other hand, when we consume fructose, the majority of it is taken up directly by the liver. This unique quality of fructose is why sugar is blamed for causing inflammation, even though this is one of fructose’s most beneficial qualities.

I know what you might be thinking: “if fructose is found in the same amount in fruit as in white table sugar, wouldn’t fruit cause inflammation too?”

While some of the hardcore anti-sugar folks do think that fruit causes inflammation, most admit that it doesn’t. But, they claim that this is only because it contains fiber, which separates it from soda, fruit juice (which is supposedly just as bad as soda), and other sugar-containing foods.

The fiber in fruit supposedly slows the absorption of fructose enough to completely abolish its toxic effects, which on the surface makes one question how toxic those effects could really be. Anyways, on to sugar and inflammation.

 

Sugar and inflammation

As I conceded in my analogy earlier, sugar can cause inflammation, which is what the anti-sugar agenda focuses on. So, let’s begin by talking about how that happens.

The liver is an extremely important and energy-intensive organ, using almost as much energy as the brain (1). It detoxifies chemicals, regulates hormones, produces digestive enzymes, and stores and releases sugar for the brain to use, among many other functions.

Fructose is our liver’s favorite fuel, which is why almost all the fructose we eat goes straight to our livers. Our livers use this fructose to produce energy, which they need a ton of to perform all their functions.

Our livers also save some of their fructose by converting it to glycogen, which is a storage form of sugar. This glycogen is extremely important because it acts as a storage form of sugar for the brain. When the brain needs more fuel, the liver breaks down the glycogen and releases it into the blood for the brain to use.

Due to the importance of storing sugar for the brain, the liver will typically store a lot of fructose in the form of glycogen – around 100 grams (this is the amount of fructose in 5 cans of soda).

But, when you feed the liver extra fructose, a couple remarkable things happen:

  • It increases the amount of fructose it burns (2).
  • It shares a large amount of the fructose with other parts of the body by releasing it as glucose and lactate, while also increasing the amount of sugar the entire body burns and stores (2, 3, 4). When this happens, the body can store as much as 1000 grams of glycogen, which is the amount of sugar in 25 cans of soda! (4) Although it should be noted that at this point you would probably have significant amounts of inflammation.

I like to think of the liver as a magic car. When you fill this car with extra gas (fructose) its engine begins to run even faster to burn the extra gas, while also sharing gas with other cars and making their engines run faster. And, the gas tank can expand to hold up to 10 times as much gas!

But, if you keep filling the car with too much gas it begins to overflow, and some of it spills out and damages the paint on the car.

This is where the inflammation comes in. If we eat so much fructose that our livers can’t burn it, share it, and store it as glycogen fast enough, it begins to overflow which causes inflammation.

But, this inflammation isn’t a bad thing! It’s a protective mechanism that stops more fuel from coming into the already-full liver.

And, this inflammation is NOT the same as the chronic inflammation seen in chronic diseases, because it’s only temporary. As the liver uses up the excess fructose (which doesn’t take long because our livers use a lot of energy), the inflammation dissipates.

 

Some concluding thoughts

Yes, sugar can cause inflammation. But, literally anything can cause inflammation depending on the dose. Water, oxygen, protein, sunlight, vitamins, minerals. This hardly constitutes the label of a “poison.”

It takes A LOT of sugar to cause inflammation. And, this isn’t the same as the chronic inflammation that goes on in chronic disease, which is due to a lack of energy.

We even have self-regulating mechanisms that stop us from consuming too much sugar. Plus, we can minimize any potential inflammatory effects of sugar by reducing PUFA consumption. (more on self-regulating sugar mechanisms and PUFA in part 2)

This is not to mention that sugar has tons of benefits. You just learned about how it fuels the liver, which is extremely important for digestion, hormone regulation, brain function, and many other processes. It also fuels the brain directly and opposes stress, as I mentioned in this article.

This isn’t to say that pure white sugar is a perfect “health food” – it’s devoid of virtually all vitamins and minerals, which can make it harmful if you’re not getting enough of these nutrients. But, it’s not the poison it’s made out to be, and just because a food contains sugar doesn’t mean that it’s unhealthy.

Fruits, fruit juice, and dried fruit, for example, are often avoided because of their sugar content. But, their sugar content is no reason to avoid them and is even a reason to eat more of them, if you ask me.

That being said, not all foods that contain sugar are healthy. Many processed foods that contain sugar also contain polyunsaturated fats and other ingredients that would most certainly exclude them from being “health foods.”

In part 2 I’ll discuss why the research behind sugar and inflammation is so misleading, as well as the role of PUFA in this inflammation and our self-regulating sugar mechanisms.

 

References

Sugar Does NOT Cause Inflammation (Part 1)

The anti-sugar agenda is stronger now than ever, and unsupported and exaggerated claims are fueling its expansion.

Sugar is blamed for everything from obesity and diabetes to heart disease and autoimmune conditions and is even considered to be “toxic” and a “poison.”

But sugar is about as far from a poison as you can get.

There are many misconceptions contributing to the demonization of sugar, one of which being that sugar causes inflammation. In the next two articles, I’m going to explain why this is not the case.

Sugar and inflammation have become inextricably linked. This inflammation is considered to be one of the most damaging effects of sugar and is believed to be at least partly responsible for sugar’s supposed role in various diseases.

But this idea is so ridiculous I don’t know where to start. It’s kind of like saying “don’t drive your car because you may drive to the hospital, and sometimes people die when they go to hospitals.” I know, it doesn’t make any sense.

Yes, people drive their cars to the hospital. And yes, people die at the hospital. But just because you drive doesn’t mean you’re going to go to the hospital, and just because people die at the hospital doesn’t mean that going to hospitals causes you to die.

In other words, eating sugar can cause inflammation. And inflammation does occur when people are unhealthy. But just because you eat sugar doesn’t mean it’s going to cause inflammation, and just because inflammation occurs when you’re unhealthy doesn’t mean that inflammation causes you to be unhealthy.

I know this all sounds a little crazy, and it is, so let me back up a bit and start by explaining what inflammation even is.

 

What is inflammation and why does it matter?

Inflammation is simply a response to damage. It acts as a signal that activates processes that stop damage from continuing.

It’s easy to think of inflammation in the context of an injury, like a cut to the skin. Once an injury like this inflicts damage, inflammation occurs which signals platelets to come and stop the bleeding.

So, inflammation is clearly not the problem, it’s just a mechanism that stops damage from continuing. But, when inflammation is chronically occurring, which happens in virtually all chronic diseases, it’s a sign that there is underlying damage that the inflammation can’t stop.

This is most common when our bodies can’t produce enough energy to handle their demands. There are a couple of reasons why this might happen:

  • We don’t have enough fuel – our bodies can’t produce energy without enough nutrients (carbs or fats, vitamins, minerals, etc.)
  • We can’t use the fuel we have – energy production can be blocked by all sorts of things, like endotoxin or polyunsaturated fats

Under these circumstances, inflammation can’t do its job of stopping the damage because the damage is a byproduct of the lack of energy, and more energy can’t be produced. This leads to the chronic inflammation that’s so often talked about as the cause of the many chronic diseases.

But, the chronic inflammation isn’t the cause of these diseases, it’s simply a byproduct of the constant damage, which is the result of a lack of energy.

So how does sugar fit into all of this?

Before we talk about that, let’s first clarify what sugar is.

 

What is Sugar?

White table sugar, or sucrose, is a carbohydrate that’s made up of 50% glucose and 50% fructose.

This is around the same ratio that’s found naturally in fruits and honey (as well as high-fructose corn syrup). In contrast, starchy carbohydrates like tubers, root vegetables, and grains contain mostly glucose with little or no fructose.

When we consume glucose, it goes to our blood and can be taken up by our entire body, including the brain, muscles, and liver.

On the other hand, when we consume fructose, the majority of it is taken up directly by the liver. This unique quality of fructose is why sugar is blamed for causing inflammation, even though this is one of fructose’s most beneficial qualities.

I know what you might be thinking: “if fructose is found in the same amount in fruit as in white table sugar, wouldn’t fruit cause inflammation too?”

While some of the hardcore anti-sugar folks do think that fruit causes inflammation, most admit that it doesn’t. But, they claim that this is only because it contains fiber, which separates it from soda, fruit juice (which is supposedly just as bad as soda), and other sugar-containing foods.

The fiber in fruit supposedly slows the absorption of fructose enough to completely abolish its toxic effects, which on the surface makes one question how toxic those effects could really be. Anyways, on to sugar and inflammation.

 

Sugar and inflammation

As I conceded in my analogy earlier, sugar can cause inflammation, which is what the anti-sugar agenda focuses on. So, let’s begin by talking about how that happens.

The liver is an extremely important and energy-intensive organ, using almost as much energy as the brain (1). It detoxifies chemicals, regulates hormones, produces digestive enzymes, and stores and releases sugar for the brain to use, among many other functions.

Fructose is our liver’s favorite fuel, which is why almost all the fructose we eat goes straight to our livers. Our livers use this fructose to produce energy, which they need a ton of to perform all their functions.

Our livers also save some of their fructose by converting it to glycogen, which is a storage form of sugar. This glycogen is extremely important because it acts as a storage form of sugar for the brain. When the brain needs more fuel, the liver breaks down the glycogen and releases it into the blood for the brain to use.

Due to the importance of storing sugar for the brain, the liver will typically store a lot of fructose in the form of glycogen – around 100 grams (this is the amount of fructose in 5 cans of soda).

But, when you feed the liver extra fructose, a couple remarkable things happen:

  • It increases the amount of fructose it burns (2).
  • It shares a large amount of the fructose with other parts of the body by releasing it as glucose and lactate, while also increasing the amount of sugar the entire body burns and stores (2, 3, 4). When this happens, the body can store as much as 1000 grams of glycogen, which is the amount of sugar in 25 cans of soda! (4) Although it should be noted that at this point you would probably have significant amounts of inflammation.

I like to think of the liver as a magic car. When you fill this car with extra gas (fructose) its engine begins to run even faster to burn the extra gas, while also sharing gas with other cars and making their engines run faster. And, the gas tank can expand to hold up to 10 times as much gas!

But, if you keep filling the car with too much gas it begins to overflow, and some of it spills out and damages the paint on the car.

This is where the inflammation comes in. If we eat so much fructose that our livers can’t burn it, share it, and store it as glycogen fast enough, it begins to overflow which causes inflammation.

But, this inflammation isn’t a bad thing! It’s a protective mechanism that stops more fuel from coming into the already-full liver.

And, this inflammation is NOT the same as the chronic inflammation seen in chronic diseases, because it’s only temporary. As the liver uses up the excess fructose (which doesn’t take long because our livers use a lot of energy), the inflammation dissipates.

 

Some concluding thoughts

Yes, sugar can cause inflammation. But, literally anything can cause inflammation depending on the dose. Water, oxygen, protein, sunlight, vitamins, minerals. This hardly constitutes the label of a “poison.”

It takes A LOT of sugar to cause inflammation. And, this isn’t the same as the chronic inflammation that goes on in chronic disease, which is due to a lack of energy.

We even have self-regulating mechanisms that stop us from consuming too much sugar. Plus, we can minimize any potential inflammatory effects of sugar by reducing PUFA consumption. (more on self-regulating sugar mechanisms and PUFA in part 2)

This is not to mention that sugar has tons of benefits. You just learned about how it fuels the liver, which is extremely important for digestion, hormone regulation, brain function, and many other processes. It also fuels the brain directly and opposes stress, as I mentioned in this article.

This isn’t to say that pure white sugar is a perfect “health food” – it’s devoid of virtually all vitamins and minerals, which can make it harmful if you’re not getting enough of these nutrients. But, it’s not the poison it’s made out to be, and just because a food contains sugar doesn’t mean that it’s unhealthy.

Fruits, fruit juice, and dried fruit, for example, are often avoided because of their sugar content. But, their sugar content is no reason to avoid them and is even a reason to eat more of them, if you ask me.

That being said, not all foods that contain sugar are healthy. Many processed foods that contain sugar also contain polyunsaturated fats and other ingredients that would most certainly exclude them from being “health foods.”

In part 2 I’ll discuss why the research behind sugar and inflammation is so misleading, as well as the role of PUFA in this inflammation and our self-regulating sugar mechanisms.

 

References

Sugar Does NOT Cause Inflammation (Part 1)

The anti-sugar agenda is stronger now than ever, and unsupported and exaggerated claims are fueling its expansion.

Sugar is blamed for everything from obesity and diabetes to heart disease and autoimmune conditions and is even considered to be “toxic” and a “poison.”

But sugar is about as far from a poison as you can get.

There are many misconceptions contributing to the demonization of sugar, one of which being that sugar causes inflammation. In the next two articles, I’m going to explain why this is not the case.

Sugar and inflammation have become inextricably linked. This inflammation is considered to be one of the most damaging effects of sugar and is believed to be at least partly responsible for sugar’s supposed role in various diseases.

But this idea is so ridiculous I don’t know where to start. It’s kind of like saying “don’t drive your car because you may drive to the hospital, and sometimes people die when they go to hospitals.” I know, it doesn’t make any sense.

Yes, people drive their cars to the hospital. And yes, people die at the hospital. But just because you drive doesn’t mean you’re going to go to the hospital, and just because people die at the hospital doesn’t mean that going to hospitals causes you to die.

In other words, eating sugar can cause inflammation. And inflammation does occur when people are unhealthy. But just because you eat sugar doesn’t mean it’s going to cause inflammation, and just because inflammation occurs when you’re unhealthy doesn’t mean that inflammation causes you to be unhealthy.

I know this all sounds a little crazy, and it is, so let me back up a bit and start by explaining what inflammation even is.

 

What is inflammation and why does it matter?

Inflammation is simply a response to damage. It acts as a signal that activates processes that stop damage from continuing.

It’s easy to think of inflammation in the context of an injury, like a cut to the skin. Once an injury like this inflicts damage, inflammation occurs which signals platelets to come and stop the bleeding.

So, inflammation is clearly not the problem, it’s just a mechanism that stops damage from continuing. But, when inflammation is chronically occurring, which happens in virtually all chronic diseases, it’s a sign that there is underlying damage that the inflammation can’t stop.

This is most common when our bodies can’t produce enough energy to handle their demands. There are a couple of reasons why this might happen:

  • We don’t have enough fuel – our bodies can’t produce energy without enough nutrients (carbs or fats, vitamins, minerals, etc.)
  • We can’t use the fuel we have – energy production can be blocked by all sorts of things, like endotoxin or polyunsaturated fats

Under these circumstances, inflammation can’t do its job of stopping the damage because the damage is a byproduct of the lack of energy, and more energy can’t be produced. This leads to the chronic inflammation that’s so often talked about as the cause of the many chronic diseases.

But, the chronic inflammation isn’t the cause of these diseases, it’s simply a byproduct of the constant damage, which is the result of a lack of energy.

So how does sugar fit into all of this?

Before we talk about that, let’s first clarify what sugar is.

 

What is Sugar?

White table sugar, or sucrose, is a carbohydrate that’s made up of 50% glucose and 50% fructose.

This is around the same ratio that’s found naturally in fruits and honey (as well as high-fructose corn syrup). In contrast, starchy carbohydrates like tubers, root vegetables, and grains contain mostly glucose with little or no fructose.

When we consume glucose, it goes to our blood and can be taken up by our entire body, including the brain, muscles, and liver.

On the other hand, when we consume fructose, the majority of it is taken up directly by the liver. This unique quality of fructose is why sugar is blamed for causing inflammation, even though this is one of fructose’s most beneficial qualities.

I know what you might be thinking: “if fructose is found in the same amount in fruit as in white table sugar, wouldn’t fruit cause inflammation too?”

While some of the hardcore anti-sugar folks do think that fruit causes inflammation, most admit that it doesn’t. But, they claim that this is only because it contains fiber, which separates it from soda, fruit juice (which is supposedly just as bad as soda), and other sugar-containing foods.

The fiber in fruit supposedly slows the absorption of fructose enough to completely abolish its toxic effects, which on the surface makes one question how toxic those effects could really be. Anyways, on to sugar and inflammation.

 

Sugar and inflammation

As I conceded in my analogy earlier, sugar can cause inflammation, which is what the anti-sugar agenda focuses on. So, let’s begin by talking about how that happens.

The liver is an extremely important and energy-intensive organ, using almost as much energy as the brain (1). It detoxifies chemicals, regulates hormones, produces digestive enzymes, and stores and releases sugar for the brain to use, among many other functions.

Fructose is our liver’s favorite fuel, which is why almost all the fructose we eat goes straight to our livers. Our livers use this fructose to produce energy, which they need a ton of to perform all their functions.

Our livers also save some of their fructose by converting it to glycogen, which is a storage form of sugar. This glycogen is extremely important because it acts as a storage form of sugar for the brain. When the brain needs more fuel, the liver breaks down the glycogen and releases it into the blood for the brain to use.

Due to the importance of storing sugar for the brain, the liver will typically store a lot of fructose in the form of glycogen – around 100 grams (this is the amount of fructose in 5 cans of soda).

But, when you feed the liver extra fructose, a couple remarkable things happen:

  • It increases the amount of fructose it burns (2).
  • It shares a large amount of the fructose with other parts of the body by releasing it as glucose and lactate, while also increasing the amount of sugar the entire body burns and stores (2, 3, 4). When this happens, the body can store as much as 1000 grams of glycogen, which is the amount of sugar in 25 cans of soda! (4) Although it should be noted that at this point you would probably have significant amounts of inflammation.

I like to think of the liver as a magic car. When you fill this car with extra gas (fructose) its engine begins to run even faster to burn the extra gas, while also sharing gas with other cars and making their engines run faster. And, the gas tank can expand to hold up to 10 times as much gas!

But, if you keep filling the car with too much gas it begins to overflow, and some of it spills out and damages the paint on the car.

This is where the inflammation comes in. If we eat so much fructose that our livers can’t burn it, share it, and store it as glycogen fast enough, it begins to overflow which causes inflammation.

But, this inflammation isn’t a bad thing! It’s a protective mechanism that stops more fuel from coming into the already-full liver.

And, this inflammation is NOT the same as the chronic inflammation seen in chronic diseases, because it’s only temporary. As the liver uses up the excess fructose (which doesn’t take long because our livers use a lot of energy), the inflammation dissipates.

 

Some concluding thoughts

Yes, sugar can cause inflammation. But, literally anything can cause inflammation depending on the dose. Water, oxygen, protein, sunlight, vitamins, minerals. This hardly constitutes the label of a “poison.”

It takes A LOT of sugar to cause inflammation. And, this isn’t the same as the chronic inflammation that goes on in chronic disease, which is due to a lack of energy.

We even have self-regulating mechanisms that stop us from consuming too much sugar. Plus, we can minimize any potential inflammatory effects of sugar by reducing PUFA consumption. (more on self-regulating sugar mechanisms and PUFA in part 2)

This is not to mention that sugar has tons of benefits. You just learned about how it fuels the liver, which is extremely important for digestion, hormone regulation, brain function, and many other processes. It also fuels the brain directly and opposes stress, as I mentioned in this article.

This isn’t to say that pure white sugar is a perfect “health food” – it’s devoid of virtually all vitamins and minerals, which can make it harmful if you’re not getting enough of these nutrients. But, it’s not the poison it’s made out to be, and just because a food contains sugar doesn’t mean that it’s unhealthy.

Fruits, fruit juice, and dried fruit, for example, are often avoided because of their sugar content. But, their sugar content is no reason to avoid them and is even a reason to eat more of them, if you ask me.

That being said, not all foods that contain sugar are healthy. Many processed foods that contain sugar also contain polyunsaturated fats and other ingredients that would most certainly exclude them from being “health foods.”

In part 2 I’ll discuss why the research behind sugar and inflammation is so misleading, as well as the role of PUFA in this inflammation and our self-regulating sugar mechanisms.

 

References

Blood Sugar, Stress, and Feeling Hangry

“You’re not you when you’re hungry.”

I don’t know how well it sells candy bars, but I do know that it’s true, and a candy bar would probably help.

The word “hangry” has become popular lately and illustrates this idea pretty well. For those who don’t know, it’s a combination of the words “hungry” and “angry,” used to describe the feeling of irritability that we get when we’re hungry.

These feelings are actually symptoms of hypoglycemia, or low blood sugar. While the idea of feeling “hangry” has been getting more publicity, the importance of blood sugar in health is still largely overlooked, at least for those who don’t have diabetes.

Like the blaming of cholesterol for heart disease, the high blood sugar seen in insulin resistance and diabetes has been mistakenly blamed as a cause of the disease, as opposed to an effect. This has led to misconceptions surrounding blood sugar, including the ideas that “high blood sugar makes people fat and causes diabetes,” “eating protein stabilizes blood sugar levels,” and “sugar is unhealthy because it raises blood sugar.

On the contrary, maintaining a higher blood sugar, or rather, avoiding low blood sugar, is important for reducing stress and plays a major role in our health. Like many other misunderstood topics, this becomes clear when we consider how blood sugar relates to energy.

Blood Sugar and Energy

Energy allows every one of our cells to function. And, to produce energy, all our cells require fuel.

While most of the cells in the human body can use either carbohydrates or fat for fuel, the cells in our brain are unique. Our brain is the most energy-intensive of all our organs, and therefore requires fuel that produces the most energy in the most efficient manner: sugar (1, 2).

Sugar, or glucose, is transported throughout our bodies and to our brains by our blood. Our blood sugar is therefore an indicator of the amount of fuel we have available, or the amount of immediate energy our bodies can produce.

If our blood sugar is high, then our bodies have a lot of fuel available. And if our blood sugar is low, then our bodies don’t have very much fuel available.

Because our brains require sugar, and we need our brains to work in order to function (and be alive), having adequate blood sugar is extremely important. But, keeping our blood sugar up is a relatively constant battle, as our blood sugar is always dropping.

Our brains are always active and are therefore always using blood sugar, which causes our blood sugar to drop slowly over time. And, when our brains or other parts of our bodies (such as muscles or organs) are highly active, like when we’re mentally or physically active, our blood sugar drops much faster.

If our blood sugar falls too low, our brains won’t have enough fuel and will shut off. So, when our blood sugar falls, our bodies adapt.

This is where feeling “hangry” comes in. We may begin to feel hungry, irritable, angry, weak, hot, nervous, anxious, jittery, or clammy (3). We also lack willpower and the ability to think as effectively (4, 5).

These effects are due to a lack of energy and are meant to reduce our blood sugar usage while also encouraging us to eat, which would raise our blood sugar. At the same time, low blood sugar activates our stress systems.

Blood Sugar and Stress

When our blood sugar drops too low, it doesn’t supply enough energy to our brains, resulting in stress. So, there are stress-induced mechanisms in place to raise our blood sugar.

The stress hormones glucagon, epinephrine (adrenaline), and growth hormone are released first (6). These hormones lead to glucose production by breaking down liver glycogen, the body’s stored form of sugar. They also switch the body’s primary fuel from sugar to fat in an effort to conserve sugar for our brains.

If these stress hormones can’t raise the blood sugar enough by breaking down liver glycogen (either because there isn’t enough glycogen or because energy is being used too quickly), then the stress hormone cortisol is released (6).

Cortisol breaks down protein, such as from muscles, organs, or other tissues, so that it can be converted to glucose through a process called gluconeogenesis. This is the last resort to raise blood sugar and supply energy.

Simply put, stress occurs when we don’t have enough energy, and then increases energy production via stress hormones. This may not sound like a big deal, but energy is integral to our health, and a lack of energy can be quite damaging.

This is evidenced by the fact that the stress hormones glucagon and cortisol are implicated in diabetes (7, 8) and that cortisol is strongly immunosuppressive and is implicated in obesity, heart disease, osteoporosis, depression and many other chronic diseases (9, 10, 11, 12).

The relationship between stress and health is acknowledged by the mainstream health community, but the relationship between blood sugar, stress, and health is not. And it’s an important one.

Blood sugar levels have an inverse relationship with stress, which makes sense considering blood sugar is an indirect measure of available energy (13, 14).

A higher blood sugar level allows us to handle greater amounts of stressors without causing stress. This relationship is so powerful that in rats with low blood sugar, certain toxins cause severe anaphylactic shock and death, while the same toxins cause only mild symptoms in rats protected by high blood sugar (16).

And, consuming carbohydrates that increase the blood sugar reduces stress that’s already occurring (14).

So, maintaining a higher, stable blood sugar will supply our brains (and the rest of our bodies) with the energy they need while inhibiting stress and the damage that comes with it.

Blood Sugar Confusion

Much of the confusion surrounding blood sugar comes from observations in people with insulin resistance or diabetes. In these cases, high blood sugar is common and is therefore blamed for some of the damage that goes on.

But, the problem in these conditions isn’t that the blood sugar is high, it’s that sugar isn’t able to be used to produce energy in the cells. Because sugar isn’t being used to produce energy, it builds up in the blood.

In these cases, the body is always under stress because it isn’t efficiently producing energy, which explains the elevated levels of glucagon and cortisol despite high blood sugar (7817).

(Note: When the ability to produce energy using sugar is inhibited or stress is already occurring, there’s no longer an inverse relationship between blood sugar and stress.)

(If you want to learn more about what actually causes type 2 diabetes and insulin resistance, check out this video.)

How to Maintain Stable Blood Sugar Levels

Maintaining a higher, stable blood sugar level supplies our bodies with the energy they need while inhibiting stress. This means improving fat loss and virtually all chronic diseases, while also preventing “hangriness.” Here are a few simple tips to help maintain a higher, stable blood sugar level throughout the day:

  • Our blood sugar is increased by carbohydrates, so eating carbohydrates allows us to maintain a higher blood sugar level and inhibits stress.
  • Our blood sugar decreases throughout the day, even at rest, and decreases even quicker when we’re physically or mentally active. So, eating a carbohydrate-containing snack or meal every 2-3 hours and after or during physical or mental activity will prevent blood sugar lows and stress.
  • Protein decreases blood sugar, so eating protein alone will cause our blood sugar to drop and stress to occur (18). But, this is easily preventable by making sure to eat carbohydrates anytime we eat protein.
References

Blood Sugar, Stress, and Feeling Hangry

“You’re not you when you’re hungry.”

I don’t know how well it sells candy bars, but I do know that it’s true, and a candy bar would probably help.

The word “hangry” has become popular lately and illustrates this idea pretty well. For those who don’t know, it’s a combination of the words “hungry” and “angry,” used to describe the feeling of irritability that we get when we’re hungry.

These feelings are actually symptoms of hypoglycemia, or low blood sugar. While the idea of feeling “hangry” has been getting more publicity, the importance of blood sugar in health is still largely overlooked, at least for those who don’t have diabetes.

Like the blaming of cholesterol for heart disease, the high blood sugar seen in insulin resistance and diabetes has been mistakenly blamed as a cause of the disease, as opposed to an effect. This has led to misconceptions surrounding blood sugar, including the ideas that “high blood sugar makes people fat and causes diabetes,” “eating protein stabilizes blood sugar levels,” and “sugar is unhealthy because it raises blood sugar.

On the contrary, maintaining a higher blood sugar, or rather, avoiding low blood sugar, is important for reducing stress and plays a major role in our health. Like many other misunderstood topics, this becomes clear when we consider how blood sugar relates to energy.

Blood Sugar and Energy

Energy allows every one of our cells to function. And, to produce energy, all our cells require fuel.

While most of the cells in the human body can use either carbohydrates or fat for fuel, the cells in our brain are unique. Our brain is the most energy-intensive of all our organs, and therefore requires fuel that produces the most energy in the most efficient manner: sugar (1, 2).

Sugar, or glucose, is transported throughout our bodies and to our brains by our blood. Our blood sugar is therefore an indicator of the amount of fuel we have available, or the amount of immediate energy our bodies can produce.

If our blood sugar is high, then our bodies have a lot of fuel available. And if our blood sugar is low, then our bodies don’t have very much fuel available.

Because our brains require sugar, and we need our brains to work in order to function (and be alive), having adequate blood sugar is extremely important. But, keeping our blood sugar up is a relatively constant battle, as our blood sugar is always dropping.

Our brains are always active and are therefore always using blood sugar, which causes our blood sugar to drop slowly over time. And, when our brains or other parts of our bodies (such as muscles or organs) are highly active, like when we’re mentally or physically active, our blood sugar drops much faster.

If our blood sugar falls too low, our brains won’t have enough fuel and will shut off. So, when our blood sugar falls, our bodies adapt.

This is where feeling “hangry” comes in. We may begin to feel hungry, irritable, angry, weak, hot, nervous, anxious, jittery, or clammy (3). We also lack willpower and the ability to think as effectively (4, 5).

These effects are due to a lack of energy and are meant to reduce our blood sugar usage while also encouraging us to eat, which would raise our blood sugar. At the same time, low blood sugar activates our stress systems.

Blood Sugar and Stress

When our blood sugar drops too low, it doesn’t supply enough energy to our brains, resulting in stress. So, there are stress-induced mechanisms in place to raise our blood sugar.

The stress hormones glucagon, epinephrine (adrenaline), and growth hormone are released first (6). These hormones lead to glucose production by breaking down liver glycogen, the body’s stored form of sugar. They also switch the body’s primary fuel from sugar to fat in an effort to conserve sugar for our brains.

If these stress hormones can’t raise the blood sugar enough by breaking down liver glycogen (either because there isn’t enough glycogen or because energy is being used too quickly), then the stress hormone cortisol is released (6).

Cortisol breaks down protein, such as from muscles, organs, or other tissues, so that it can be converted to glucose through a process called gluconeogenesis. This is the last resort to raise blood sugar and supply energy.

Simply put, stress occurs when we don’t have enough energy, and then increases energy production via stress hormones. This may not sound like a big deal, but energy is integral to our health, and a lack of energy can be quite damaging.

This is evidenced by the fact that the stress hormones glucagon and cortisol are implicated in diabetes (7, 8) and that cortisol is strongly immunosuppressive and is implicated in obesity, heart disease, osteoporosis, depression and many other chronic diseases (9, 10, 11, 12).

The relationship between stress and health is acknowledged by the mainstream health community, but the relationship between blood sugar, stress, and health is not. And it’s an important one.

Blood sugar levels have an inverse relationship with stress, which makes sense considering blood sugar is an indirect measure of available energy (13, 14).

A higher blood sugar level allows us to handle greater amounts of stressors without causing stress. This relationship is so powerful that in rats with low blood sugar, certain toxins cause severe anaphylactic shock and death, while the same toxins cause only mild symptoms in rats protected by high blood sugar (16).

And, consuming carbohydrates that increase the blood sugar reduces stress that’s already occurring (14).

So, maintaining a higher, stable blood sugar will supply our brains (and the rest of our bodies) with the energy they need while inhibiting stress and the damage that comes with it.

Blood Sugar Confusion

Much of the confusion surrounding blood sugar comes from observations in people with insulin resistance or diabetes. In these cases, high blood sugar is common and is therefore blamed for some of the damage that goes on.

But, the problem in these conditions isn’t that the blood sugar is high, it’s that sugar isn’t able to be used to produce energy in the cells. Because sugar isn’t being used to produce energy, it builds up in the blood.

In these cases, the body is always under stress because it isn’t efficiently producing energy, which explains the elevated levels of glucagon and cortisol despite high blood sugar (7817).

(Note: When the ability to produce energy using sugar is inhibited or stress is already occurring, there’s no longer an inverse relationship between blood sugar and stress.)

(If you want to learn more about what actually causes type 2 diabetes and insulin resistance, check out this video.)

How to Maintain Stable Blood Sugar Levels

Maintaining a higher, stable blood sugar level supplies our bodies with the energy they need while inhibiting stress. This means improving fat loss and virtually all chronic diseases, while also preventing “hangriness.” Here are a few simple tips to help maintain a higher, stable blood sugar level throughout the day:

  • Our blood sugar is increased by carbohydrates, so eating carbohydrates allows us to maintain a higher blood sugar level and inhibits stress.
  • Our blood sugar decreases throughout the day, even at rest, and decreases even quicker when we’re physically or mentally active. So, eating a carbohydrate-containing snack or meal every 2-3 hours and after or during physical or mental activity will prevent blood sugar lows and stress.
  • Protein decreases blood sugar, so eating protein alone will cause our blood sugar to drop and stress to occur (18). But, this is easily preventable by making sure to eat carbohydrates anytime we eat protein.
References

Blood Sugar, Stress, and Feeling Hangry

“You’re not you when you’re hungry.”

I don’t know how well it sells candy bars, but I do know that it’s true, and a candy bar would probably help.

The word “hangry” has become popular lately and illustrates this idea pretty well. For those who don’t know, it’s a combination of the words “hungry” and “angry,” used to describe the feeling of irritability that we get when we’re hungry.

These feelings are actually symptoms of hypoglycemia, or low blood sugar. While the idea of feeling “hangry” has been getting more publicity, the importance of blood sugar in health is still largely overlooked, at least for those who don’t have diabetes.

Like the blaming of cholesterol for heart disease, the high blood sugar seen in insulin resistance and diabetes has been mistakenly blamed as a cause of the disease, as opposed to an effect. This has led to misconceptions surrounding blood sugar, including the ideas that “high blood sugar makes people fat and causes diabetes,” “eating protein stabilizes blood sugar levels,” and “sugar is unhealthy because it raises blood sugar.

On the contrary, maintaining a higher blood sugar, or rather, avoiding low blood sugar, is important for reducing stress and plays a major role in our health. Like many other misunderstood topics, this becomes clear when we consider how blood sugar relates to energy.

Blood Sugar and Energy

Energy allows every one of our cells to function. And, to produce energy, all our cells require fuel.

While most of the cells in the human body can use either carbohydrates or fat for fuel, the cells in our brain are unique. Our brain is the most energy-intensive of all our organs, and therefore requires fuel that produces the most energy in the most efficient manner: sugar (1, 2).

Sugar, or glucose, is transported throughout our bodies and to our brains by our blood. Our blood sugar is therefore an indicator of the amount of fuel we have available, or the amount of immediate energy our bodies can produce.

If our blood sugar is high, then our bodies have a lot of fuel available. And if our blood sugar is low, then our bodies don’t have very much fuel available.

Because our brains require sugar, and we need our brains to work in order to function (and be alive), having adequate blood sugar is extremely important. But, keeping our blood sugar up is a relatively constant battle, as our blood sugar is always dropping.

Our brains are always active and are therefore always using blood sugar, which causes our blood sugar to drop slowly over time. And, when our brains or other parts of our bodies (such as muscles or organs) are highly active, like when we’re mentally or physically active, our blood sugar drops much faster.

If our blood sugar falls too low, our brains won’t have enough fuel and will shut off. So, when our blood sugar falls, our bodies adapt.

This is where feeling “hangry” comes in. We may begin to feel hungry, irritable, angry, weak, hot, nervous, anxious, jittery, or clammy (3). We also lack willpower and the ability to think as effectively (4, 5).

These effects are due to a lack of energy and are meant to reduce our blood sugar usage while also encouraging us to eat, which would raise our blood sugar. At the same time, low blood sugar activates our stress systems.

Blood Sugar and Stress

When our blood sugar drops too low, it doesn’t supply enough energy to our brains, resulting in stress. So, there are stress-induced mechanisms in place to raise our blood sugar.

The stress hormones glucagon, epinephrine (adrenaline), and growth hormone are released first (6). These hormones lead to glucose production by breaking down liver glycogen, the body’s stored form of sugar. They also switch the body’s primary fuel from sugar to fat in an effort to conserve sugar for our brains.

If these stress hormones can’t raise the blood sugar enough by breaking down liver glycogen (either because there isn’t enough glycogen or because energy is being used too quickly), then the stress hormone cortisol is released (6).

Cortisol breaks down protein, such as from muscles, organs, or other tissues, so that it can be converted to glucose through a process called gluconeogenesis. This is the last resort to raise blood sugar and supply energy.

Simply put, stress occurs when we don’t have enough energy, and then increases energy production via stress hormones. This may not sound like a big deal, but energy is integral to our health, and a lack of energy can be quite damaging.

This is evidenced by the fact that the stress hormones glucagon and cortisol are implicated in diabetes (7, 8) and that cortisol is strongly immunosuppressive and is implicated in obesity, heart disease, osteoporosis, depression and many other chronic diseases (9, 10, 11, 12).

The relationship between stress and health is acknowledged by the mainstream health community, but the relationship between blood sugar, stress, and health is not. And it’s an important one.

Blood sugar levels have an inverse relationship with stress, which makes sense considering blood sugar is an indirect measure of available energy (13, 14).

A higher blood sugar level allows us to handle greater amounts of stressors without causing stress. This relationship is so powerful that in rats with low blood sugar, certain toxins cause severe anaphylactic shock and death, while the same toxins cause only mild symptoms in rats protected by high blood sugar (16).

And, consuming carbohydrates that increase the blood sugar reduces stress that’s already occurring (14).

So, maintaining a higher, stable blood sugar will supply our brains (and the rest of our bodies) with the energy they need while inhibiting stress and the damage that comes with it.

Blood Sugar Confusion

Much of the confusion surrounding blood sugar comes from observations in people with insulin resistance or diabetes. In these cases, high blood sugar is common and is therefore blamed for some of the damage that goes on.

But, the problem in these conditions isn’t that the blood sugar is high, it’s that sugar isn’t able to be used to produce energy in the cells. Because sugar isn’t being used to produce energy, it builds up in the blood.

In these cases, the body is always under stress because it isn’t efficiently producing energy, which explains the elevated levels of glucagon and cortisol despite high blood sugar (7817).

(Note: When the ability to produce energy using sugar is inhibited or stress is already occurring, there’s no longer an inverse relationship between blood sugar and stress.)

(If you want to learn more about what actually causes type 2 diabetes and insulin resistance, check out this video.)

How to Maintain Stable Blood Sugar Levels

Maintaining a higher, stable blood sugar level supplies our bodies with the energy they need while inhibiting stress. This means improving fat loss and virtually all chronic diseases, while also preventing “hangriness.” Here are a few simple tips to help maintain a higher, stable blood sugar level throughout the day:

  • Our blood sugar is increased by carbohydrates, so eating carbohydrates allows us to maintain a higher blood sugar level and inhibits stress.
  • Our blood sugar decreases throughout the day, even at rest, and decreases even quicker when we’re physically or mentally active. So, eating a carbohydrate-containing snack or meal every 2-3 hours and after or during physical or mental activity will prevent blood sugar lows and stress.
  • Protein decreases blood sugar, so eating protein alone will cause our blood sugar to drop and stress to occur (18). But, this is easily preventable by making sure to eat carbohydrates anytime we eat protein.
References

Blood Sugar, Stress, and Feeling Hangry

“You’re not you when you’re hungry.”

I don’t know how well it sells candy bars, but I do know that it’s true, and a candy bar would probably help.

The word “hangry” has become popular lately and illustrates this idea pretty well. For those who don’t know, it’s a combination of the words “hungry” and “angry,” used to describe the feeling of irritability that we get when we’re hungry.

These feelings are actually symptoms of hypoglycemia, or low blood sugar. While the idea of feeling “hangry” has been getting more publicity, the importance of blood sugar in health is still largely overlooked, at least for those who don’t have diabetes.

Like the blaming of cholesterol for heart disease, the high blood sugar seen in insulin resistance and diabetes has been mistakenly blamed as a cause of the disease, as opposed to an effect. This has led to misconceptions surrounding blood sugar, including the ideas that “high blood sugar makes people fat and causes diabetes,” “eating protein stabilizes blood sugar levels,” and “sugar is unhealthy because it raises blood sugar.

On the contrary, maintaining a higher blood sugar, or rather, avoiding low blood sugar, is important for reducing stress and plays a major role in our health. Like many other misunderstood topics, this becomes clear when we consider how blood sugar relates to energy.

Blood Sugar and Energy

Energy allows every one of our cells to function. And, to produce energy, all our cells require fuel.

While most of the cells in the human body can use either carbohydrates or fat for fuel, the cells in our brain are unique. Our brain is the most energy-intensive of all our organs, and therefore requires fuel that produces the most energy in the most efficient manner: sugar (1, 2).

Sugar, or glucose, is transported throughout our bodies and to our brains by our blood. Our blood sugar is therefore an indicator of the amount of fuel we have available, or the amount of immediate energy our bodies can produce.

If our blood sugar is high, then our bodies have a lot of fuel available. And if our blood sugar is low, then our bodies don’t have very much fuel available.

Because our brains require sugar, and we need our brains to work in order to function (and be alive), having adequate blood sugar is extremely important. But, keeping our blood sugar up is a relatively constant battle, as our blood sugar is always dropping.

Our brains are always active and are therefore always using blood sugar, which causes our blood sugar to drop slowly over time. And, when our brains or other parts of our bodies (such as muscles or organs) are highly active, like when we’re mentally or physically active, our blood sugar drops much faster.

If our blood sugar falls too low, our brains won’t have enough fuel and will shut off. So, when our blood sugar falls, our bodies adapt.

This is where feeling “hangry” comes in. We may begin to feel hungry, irritable, angry, weak, hot, nervous, anxious, jittery, or clammy (3). We also lack willpower and the ability to think as effectively (4, 5).

These effects are due to a lack of energy and are meant to reduce our blood sugar usage while also encouraging us to eat, which would raise our blood sugar. At the same time, low blood sugar activates our stress systems.

Blood Sugar and Stress

When our blood sugar drops too low, it doesn’t supply enough energy to our brains, resulting in stress. So, there are stress-induced mechanisms in place to raise our blood sugar.

The stress hormones glucagon, epinephrine (adrenaline), and growth hormone are released first (6). These hormones lead to glucose production by breaking down liver glycogen, the body’s stored form of sugar. They also switch the body’s primary fuel from sugar to fat in an effort to conserve sugar for our brains.

If these stress hormones can’t raise the blood sugar enough by breaking down liver glycogen (either because there isn’t enough glycogen or because energy is being used too quickly), then the stress hormone cortisol is released (6).

Cortisol breaks down protein, such as from muscles, organs, or other tissues, so that it can be converted to glucose through a process called gluconeogenesis. This is the last resort to raise blood sugar and supply energy.

Simply put, stress occurs when we don’t have enough energy, and then increases energy production via stress hormones. This may not sound like a big deal, but energy is integral to our health, and a lack of energy can be quite damaging.

This is evidenced by the fact that the stress hormones glucagon and cortisol are implicated in diabetes (7, 8) and that cortisol is strongly immunosuppressive and is implicated in obesity, heart disease, osteoporosis, depression and many other chronic diseases (9, 10, 11, 12).

The relationship between stress and health is acknowledged by the mainstream health community, but the relationship between blood sugar, stress, and health is not. And it’s an important one.

Blood sugar levels have an inverse relationship with stress, which makes sense considering blood sugar is an indirect measure of available energy (13, 14).

A higher blood sugar level allows us to handle greater amounts of stressors without causing stress. This relationship is so powerful that in rats with low blood sugar, certain toxins cause severe anaphylactic shock and death, while the same toxins cause only mild symptoms in rats protected by high blood sugar (16).

And, consuming carbohydrates that increase the blood sugar reduces stress that’s already occurring (14).

So, maintaining a higher, stable blood sugar will supply our brains (and the rest of our bodies) with the energy they need while inhibiting stress and the damage that comes with it.

Blood Sugar Confusion

Much of the confusion surrounding blood sugar comes from observations in people with insulin resistance or diabetes. In these cases, high blood sugar is common and is therefore blamed for some of the damage that goes on.

But, the problem in these conditions isn’t that the blood sugar is high, it’s that sugar isn’t able to be used to produce energy in the cells. Because sugar isn’t being used to produce energy, it builds up in the blood.

In these cases, the body is always under stress because it isn’t efficiently producing energy, which explains the elevated levels of glucagon and cortisol despite high blood sugar (7817).

(Note: When the ability to produce energy using sugar is inhibited or stress is already occurring, there’s no longer an inverse relationship between blood sugar and stress.)

(If you want to learn more about what actually causes type 2 diabetes and insulin resistance, check out this video.)

How to Maintain Stable Blood Sugar Levels

Maintaining a higher, stable blood sugar level supplies our bodies with the energy they need while inhibiting stress. This means improving fat loss and virtually all chronic diseases, while also preventing “hangriness.” Here are a few simple tips to help maintain a higher, stable blood sugar level throughout the day:

  • Our blood sugar is increased by carbohydrates, so eating carbohydrates allows us to maintain a higher blood sugar level and inhibits stress.
  • Our blood sugar decreases throughout the day, even at rest, and decreases even quicker when we’re physically or mentally active. So, eating a carbohydrate-containing snack or meal every 2-3 hours and after or during physical or mental activity will prevent blood sugar lows and stress.
  • Protein decreases blood sugar, so eating protein alone will cause our blood sugar to drop and stress to occur (18). But, this is easily preventable by making sure to eat carbohydrates anytime we eat protein.
References

Blood Sugar, Stress, and Feeling Hangry

“You’re not you when you’re hungry.”

I don’t know how well it sells candy bars, but I do know that it’s true, and a candy bar would probably help.

The word “hangry” has become popular lately and illustrates this idea pretty well. For those who don’t know, it’s a combination of the words “hungry” and “angry,” used to describe the feeling of irritability that we get when we’re hungry.

These feelings are actually symptoms of hypoglycemia, or low blood sugar. While the idea of feeling “hangry” has been getting more publicity, the importance of blood sugar in health is still largely overlooked, at least for those who don’t have diabetes.

Like the blaming of cholesterol for heart disease, the high blood sugar seen in insulin resistance and diabetes has been mistakenly blamed as a cause of the disease, as opposed to an effect. This has led to misconceptions surrounding blood sugar, including the ideas that “high blood sugar makes people fat and causes diabetes,” “eating protein stabilizes blood sugar levels,” and “sugar is unhealthy because it raises blood sugar.

On the contrary, maintaining a higher blood sugar, or rather, avoiding low blood sugar, is important for reducing stress and plays a major role in our health. Like many other misunderstood topics, this becomes clear when we consider how blood sugar relates to energy.

Blood Sugar and Energy

Energy allows every one of our cells to function. And, to produce energy, all our cells require fuel.

While most of the cells in the human body can use either carbohydrates or fat for fuel, the cells in our brain are unique. Our brain is the most energy-intensive of all our organs, and therefore requires fuel that produces the most energy in the most efficient manner: sugar (1, 2).

Sugar, or glucose, is transported throughout our bodies and to our brains by our blood. Our blood sugar is therefore an indicator of the amount of fuel we have available, or the amount of immediate energy our bodies can produce.

If our blood sugar is high, then our bodies have a lot of fuel available. And if our blood sugar is low, then our bodies don’t have very much fuel available.

Because our brains require sugar, and we need our brains to work in order to function (and be alive), having adequate blood sugar is extremely important. But, keeping our blood sugar up is a relatively constant battle, as our blood sugar is always dropping.

Our brains are always active and are therefore always using blood sugar, which causes our blood sugar to drop slowly over time. And, when our brains or other parts of our bodies (such as muscles or organs) are highly active, like when we’re mentally or physically active, our blood sugar drops much faster.

If our blood sugar falls too low, our brains won’t have enough fuel and will shut off. So, when our blood sugar falls, our bodies adapt.

This is where feeling “hangry” comes in. We may begin to feel hungry, irritable, angry, weak, hot, nervous, anxious, jittery, or clammy (3). We also lack willpower and the ability to think as effectively (4, 5).

These effects are due to a lack of energy and are meant to reduce our blood sugar usage while also encouraging us to eat, which would raise our blood sugar. At the same time, low blood sugar activates our stress systems.

Blood Sugar and Stress

When our blood sugar drops too low, it doesn’t supply enough energy to our brains, resulting in stress. So, there are stress-induced mechanisms in place to raise our blood sugar.

The stress hormones glucagon, epinephrine (adrenaline), and growth hormone are released first (6). These hormones lead to glucose production by breaking down liver glycogen, the body’s stored form of sugar. They also switch the body’s primary fuel from sugar to fat in an effort to conserve sugar for our brains.

If these stress hormones can’t raise the blood sugar enough by breaking down liver glycogen (either because there isn’t enough glycogen or because energy is being used too quickly), then the stress hormone cortisol is released (6).

Cortisol breaks down protein, such as from muscles, organs, or other tissues, so that it can be converted to glucose through a process called gluconeogenesis. This is the last resort to raise blood sugar and supply energy.

Simply put, stress occurs when we don’t have enough energy, and then increases energy production via stress hormones. This may not sound like a big deal, but energy is integral to our health, and a lack of energy can be quite damaging.

This is evidenced by the fact that the stress hormones glucagon and cortisol are implicated in diabetes (7, 8) and that cortisol is strongly immunosuppressive and is implicated in obesity, heart disease, osteoporosis, depression and many other chronic diseases (9, 10, 11, 12).

The relationship between stress and health is acknowledged by the mainstream health community, but the relationship between blood sugar, stress, and health is not. And it’s an important one.

Blood sugar levels have an inverse relationship with stress, which makes sense considering blood sugar is an indirect measure of available energy (13, 14).

A higher blood sugar level allows us to handle greater amounts of stressors without causing stress. This relationship is so powerful that in rats with low blood sugar, certain toxins cause severe anaphylactic shock and death, while the same toxins cause only mild symptoms in rats protected by high blood sugar (16).

And, consuming carbohydrates that increase the blood sugar reduces stress that’s already occurring (14).

So, maintaining a higher, stable blood sugar will supply our brains (and the rest of our bodies) with the energy they need while inhibiting stress and the damage that comes with it.

Blood Sugar Confusion

Much of the confusion surrounding blood sugar comes from observations in people with insulin resistance or diabetes. In these cases, high blood sugar is common and is therefore blamed for some of the damage that goes on.

But, the problem in these conditions isn’t that the blood sugar is high, it’s that sugar isn’t able to be used to produce energy in the cells. Because sugar isn’t being used to produce energy, it builds up in the blood.

In these cases, the body is always under stress because it isn’t efficiently producing energy, which explains the elevated levels of glucagon and cortisol despite high blood sugar (7817).

(Note: When the ability to produce energy using sugar is inhibited or stress is already occurring, there’s no longer an inverse relationship between blood sugar and stress.)

(If you want to learn more about what actually causes type 2 diabetes and insulin resistance, check out this video.)

How to Maintain Stable Blood Sugar Levels

Maintaining a higher, stable blood sugar level supplies our bodies with the energy they need while inhibiting stress. This means improving fat loss and virtually all chronic diseases, while also preventing “hangriness.” Here are a few simple tips to help maintain a higher, stable blood sugar level throughout the day:

  • Our blood sugar is increased by carbohydrates, so eating carbohydrates allows us to maintain a higher blood sugar level and inhibits stress.
  • Our blood sugar decreases throughout the day, even at rest, and decreases even quicker when we’re physically or mentally active. So, eating a carbohydrate-containing snack or meal every 2-3 hours and after or during physical or mental activity will prevent blood sugar lows and stress.
  • Protein decreases blood sugar, so eating protein alone will cause our blood sugar to drop and stress to occur (18). But, this is easily preventable by making sure to eat carbohydrates anytime we eat protein.
References

Blood Sugar, Stress, and Feeling Hangry

“You’re not you when you’re hungry.”

I don’t know how well it sells candy bars, but I do know that it’s true, and a candy bar would probably help.

The word “hangry” has become popular lately and illustrates this idea pretty well. For those who don’t know, it’s a combination of the words “hungry” and “angry,” used to describe the feeling of irritability that we get when we’re hungry.

These feelings are actually symptoms of hypoglycemia, or low blood sugar. While the idea of feeling “hangry” has been getting more publicity, the importance of blood sugar in health is still largely overlooked, at least for those who don’t have diabetes.

Like the blaming of cholesterol for heart disease, the high blood sugar seen in insulin resistance and diabetes has been mistakenly blamed as a cause of the disease, as opposed to an effect. This has led to misconceptions surrounding blood sugar, including the ideas that “high blood sugar makes people fat and causes diabetes,” “eating protein stabilizes blood sugar levels,” and “sugar is unhealthy because it raises blood sugar.

On the contrary, maintaining a higher blood sugar, or rather, avoiding low blood sugar, is important for reducing stress and plays a major role in our health. Like many other misunderstood topics, this becomes clear when we consider how blood sugar relates to energy.

Blood Sugar and Energy

Energy allows every one of our cells to function. And, to produce energy, all our cells require fuel.

While most of the cells in the human body can use either carbohydrates or fat for fuel, the cells in our brain are unique. Our brain is the most energy-intensive of all our organs, and therefore requires fuel that produces the most energy in the most efficient manner: sugar (1, 2).

Sugar, or glucose, is transported throughout our bodies and to our brains by our blood. Our blood sugar is therefore an indicator of the amount of fuel we have available, or the amount of immediate energy our bodies can produce.

If our blood sugar is high, then our bodies have a lot of fuel available. And if our blood sugar is low, then our bodies don’t have very much fuel available.

Because our brains require sugar, and we need our brains to work in order to function (and be alive), having adequate blood sugar is extremely important. But, keeping our blood sugar up is a relatively constant battle, as our blood sugar is always dropping.

Our brains are always active and are therefore always using blood sugar, which causes our blood sugar to drop slowly over time. And, when our brains or other parts of our bodies (such as muscles or organs) are highly active, like when we’re mentally or physically active, our blood sugar drops much faster.

If our blood sugar falls too low, our brains won’t have enough fuel and will shut off. So, when our blood sugar falls, our bodies adapt.

This is where feeling “hangry” comes in. We may begin to feel hungry, irritable, angry, weak, hot, nervous, anxious, jittery, or clammy (3). We also lack willpower and the ability to think as effectively (4, 5).

These effects are due to a lack of energy and are meant to reduce our blood sugar usage while also encouraging us to eat, which would raise our blood sugar. At the same time, low blood sugar activates our stress systems.

Blood Sugar and Stress

When our blood sugar drops too low, it doesn’t supply enough energy to our brains, resulting in stress. So, there are stress-induced mechanisms in place to raise our blood sugar.

The stress hormones glucagon, epinephrine (adrenaline), and growth hormone are released first (6). These hormones lead to glucose production by breaking down liver glycogen, the body’s stored form of sugar. They also switch the body’s primary fuel from sugar to fat in an effort to conserve sugar for our brains.

If these stress hormones can’t raise the blood sugar enough by breaking down liver glycogen (either because there isn’t enough glycogen or because energy is being used too quickly), then the stress hormone cortisol is released (6).

Cortisol breaks down protein, such as from muscles, organs, or other tissues, so that it can be converted to glucose through a process called gluconeogenesis. This is the last resort to raise blood sugar and supply energy.

Simply put, stress occurs when we don’t have enough energy, and then increases energy production via stress hormones. This may not sound like a big deal, but energy is integral to our health, and a lack of energy can be quite damaging.

This is evidenced by the fact that the stress hormones glucagon and cortisol are implicated in diabetes (7, 8) and that cortisol is strongly immunosuppressive and is implicated in obesity, heart disease, osteoporosis, depression and many other chronic diseases (9, 10, 11, 12).

The relationship between stress and health is acknowledged by the mainstream health community, but the relationship between blood sugar, stress, and health is not. And it’s an important one.

Blood sugar levels have an inverse relationship with stress, which makes sense considering blood sugar is an indirect measure of available energy (13, 14).

A higher blood sugar level allows us to handle greater amounts of stressors without causing stress. This relationship is so powerful that in rats with low blood sugar, certain toxins cause severe anaphylactic shock and death, while the same toxins cause only mild symptoms in rats protected by high blood sugar (16).

And, consuming carbohydrates that increase the blood sugar reduces stress that’s already occurring (14).

So, maintaining a higher, stable blood sugar will supply our brains (and the rest of our bodies) with the energy they need while inhibiting stress and the damage that comes with it.

Blood Sugar Confusion

Much of the confusion surrounding blood sugar comes from observations in people with insulin resistance or diabetes. In these cases, high blood sugar is common and is therefore blamed for some of the damage that goes on.

But, the problem in these conditions isn’t that the blood sugar is high, it’s that sugar isn’t able to be used to produce energy in the cells. Because sugar isn’t being used to produce energy, it builds up in the blood.

In these cases, the body is always under stress because it isn’t efficiently producing energy, which explains the elevated levels of glucagon and cortisol despite high blood sugar (7817).

(Note: When the ability to produce energy using sugar is inhibited or stress is already occurring, there’s no longer an inverse relationship between blood sugar and stress.)

(If you want to learn more about what actually causes type 2 diabetes and insulin resistance, check out this video.)

How to Maintain Stable Blood Sugar Levels

Maintaining a higher, stable blood sugar level supplies our bodies with the energy they need while inhibiting stress. This means improving fat loss and virtually all chronic diseases, while also preventing “hangriness.” Here are a few simple tips to help maintain a higher, stable blood sugar level throughout the day:

  • Our blood sugar is increased by carbohydrates, so eating carbohydrates allows us to maintain a higher blood sugar level and inhibits stress.
  • Our blood sugar decreases throughout the day, even at rest, and decreases even quicker when we’re physically or mentally active. So, eating a carbohydrate-containing snack or meal every 2-3 hours and after or during physical or mental activity will prevent blood sugar lows and stress.
  • Protein decreases blood sugar, so eating protein alone will cause our blood sugar to drop and stress to occur (18). But, this is easily preventable by making sure to eat carbohydrates anytime we eat protein.
References

Blood Sugar, Stress, and Feeling Hangry

“You’re not you when you’re hungry.”

I don’t know how well it sells candy bars, but I do know that it’s true, and a candy bar would probably help.

The word “hangry” has become popular lately and illustrates this idea pretty well. For those who don’t know, it’s a combination of the words “hungry” and “angry,” used to describe the feeling of irritability that we get when we’re hungry.

These feelings are actually symptoms of hypoglycemia, or low blood sugar. While the idea of feeling “hangry” has been getting more publicity, the importance of blood sugar in health is still largely overlooked, at least for those who don’t have diabetes.

Like the blaming of cholesterol for heart disease, the high blood sugar seen in insulin resistance and diabetes has been mistakenly blamed as a cause of the disease, as opposed to an effect. This has led to misconceptions surrounding blood sugar, including the ideas that “high blood sugar makes people fat and causes diabetes,” “eating protein stabilizes blood sugar levels,” and “sugar is unhealthy because it raises blood sugar.

On the contrary, maintaining a higher blood sugar, or rather, avoiding low blood sugar, is important for reducing stress and plays a major role in our health. Like many other misunderstood topics, this becomes clear when we consider how blood sugar relates to energy.

Blood Sugar and Energy

Energy allows every one of our cells to function. And, to produce energy, all our cells require fuel.

While most of the cells in the human body can use either carbohydrates or fat for fuel, the cells in our brain are unique. Our brain is the most energy-intensive of all our organs, and therefore requires fuel that produces the most energy in the most efficient manner: sugar (1, 2).

Sugar, or glucose, is transported throughout our bodies and to our brains by our blood. Our blood sugar is therefore an indicator of the amount of fuel we have available, or the amount of immediate energy our bodies can produce.

If our blood sugar is high, then our bodies have a lot of fuel available. And if our blood sugar is low, then our bodies don’t have very much fuel available.

Because our brains require sugar, and we need our brains to work in order to function (and be alive), having adequate blood sugar is extremely important. But, keeping our blood sugar up is a relatively constant battle, as our blood sugar is always dropping.

Our brains are always active and are therefore always using blood sugar, which causes our blood sugar to drop slowly over time. And, when our brains or other parts of our bodies (such as muscles or organs) are highly active, like when we’re mentally or physically active, our blood sugar drops much faster.

If our blood sugar falls too low, our brains won’t have enough fuel and will shut off. So, when our blood sugar falls, our bodies adapt.

This is where feeling “hangry” comes in. We may begin to feel hungry, irritable, angry, weak, hot, nervous, anxious, jittery, or clammy (3). We also lack willpower and the ability to think as effectively (4, 5).

These effects are due to a lack of energy and are meant to reduce our blood sugar usage while also encouraging us to eat, which would raise our blood sugar. At the same time, low blood sugar activates our stress systems.

Blood Sugar and Stress

When our blood sugar drops too low, it doesn’t supply enough energy to our brains, resulting in stress. So, there are stress-induced mechanisms in place to raise our blood sugar.

The stress hormones glucagon, epinephrine (adrenaline), and growth hormone are released first (6). These hormones lead to glucose production by breaking down liver glycogen, the body’s stored form of sugar. They also switch the body’s primary fuel from sugar to fat in an effort to conserve sugar for our brains.

If these stress hormones can’t raise the blood sugar enough by breaking down liver glycogen (either because there isn’t enough glycogen or because energy is being used too quickly), then the stress hormone cortisol is released (6).

Cortisol breaks down protein, such as from muscles, organs, or other tissues, so that it can be converted to glucose through a process called gluconeogenesis. This is the last resort to raise blood sugar and supply energy.

Simply put, stress occurs when we don’t have enough energy, and then increases energy production via stress hormones. This may not sound like a big deal, but energy is integral to our health, and a lack of energy can be quite damaging.

This is evidenced by the fact that the stress hormones glucagon and cortisol are implicated in diabetes (7, 8) and that cortisol is strongly immunosuppressive and is implicated in obesity, heart disease, osteoporosis, depression and many other chronic diseases (9, 10, 11, 12).

The relationship between stress and health is acknowledged by the mainstream health community, but the relationship between blood sugar, stress, and health is not. And it’s an important one.

Blood sugar levels have an inverse relationship with stress, which makes sense considering blood sugar is an indirect measure of available energy (13, 14).

A higher blood sugar level allows us to handle greater amounts of stressors without causing stress. This relationship is so powerful that in rats with low blood sugar, certain toxins cause severe anaphylactic shock and death, while the same toxins cause only mild symptoms in rats protected by high blood sugar (16).

And, consuming carbohydrates that increase the blood sugar reduces stress that’s already occurring (14).

So, maintaining a higher, stable blood sugar will supply our brains (and the rest of our bodies) with the energy they need while inhibiting stress and the damage that comes with it.

Blood Sugar Confusion

Much of the confusion surrounding blood sugar comes from observations in people with insulin resistance or diabetes. In these cases, high blood sugar is common and is therefore blamed for some of the damage that goes on.

But, the problem in these conditions isn’t that the blood sugar is high, it’s that sugar isn’t able to be used to produce energy in the cells. Because sugar isn’t being used to produce energy, it builds up in the blood.

In these cases, the body is always under stress because it isn’t efficiently producing energy, which explains the elevated levels of glucagon and cortisol despite high blood sugar (7817).

(Note: When the ability to produce energy using sugar is inhibited or stress is already occurring, there’s no longer an inverse relationship between blood sugar and stress.)

(If you want to learn more about what actually causes type 2 diabetes and insulin resistance, check out this video.)

How to Maintain Stable Blood Sugar Levels

Maintaining a higher, stable blood sugar level supplies our bodies with the energy they need while inhibiting stress. This means improving fat loss and virtually all chronic diseases, while also preventing “hangriness.” Here are a few simple tips to help maintain a higher, stable blood sugar level throughout the day:

  • Our blood sugar is increased by carbohydrates, so eating carbohydrates allows us to maintain a higher blood sugar level and inhibits stress.
  • Our blood sugar decreases throughout the day, even at rest, and decreases even quicker when we’re physically or mentally active. So, eating a carbohydrate-containing snack or meal every 2-3 hours and after or during physical or mental activity will prevent blood sugar lows and stress.
  • Protein decreases blood sugar, so eating protein alone will cause our blood sugar to drop and stress to occur (18). But, this is easily preventable by making sure to eat carbohydrates anytime we eat protein.
References

Blood Sugar, Stress, and Feeling Hangry

“You’re not you when you’re hungry.”

I don’t know how well it sells candy bars, but I do know that it’s true, and a candy bar would probably help.

The word “hangry” has become popular lately and illustrates this idea pretty well. For those who don’t know, it’s a combination of the words “hungry” and “angry,” used to describe the feeling of irritability that we get when we’re hungry.

These feelings are actually symptoms of hypoglycemia, or low blood sugar. While the idea of feeling “hangry” has been getting more publicity, the importance of blood sugar in health is still largely overlooked, at least for those who don’t have diabetes.

Like the blaming of cholesterol for heart disease, the high blood sugar seen in insulin resistance and diabetes has been mistakenly blamed as a cause of the disease, as opposed to an effect. This has led to misconceptions surrounding blood sugar, including the ideas that “high blood sugar makes people fat and causes diabetes,” “eating protein stabilizes blood sugar levels,” and “sugar is unhealthy because it raises blood sugar.

On the contrary, maintaining a higher blood sugar, or rather, avoiding low blood sugar, is important for reducing stress and plays a major role in our health. Like many other misunderstood topics, this becomes clear when we consider how blood sugar relates to energy.

Blood Sugar and Energy

Energy allows every one of our cells to function. And, to produce energy, all our cells require fuel.

While most of the cells in the human body can use either carbohydrates or fat for fuel, the cells in our brain are unique. Our brain is the most energy-intensive of all our organs, and therefore requires fuel that produces the most energy in the most efficient manner: sugar (1, 2).

Sugar, or glucose, is transported throughout our bodies and to our brains by our blood. Our blood sugar is therefore an indicator of the amount of fuel we have available, or the amount of immediate energy our bodies can produce.

If our blood sugar is high, then our bodies have a lot of fuel available. And if our blood sugar is low, then our bodies don’t have very much fuel available.

Because our brains require sugar, and we need our brains to work in order to function (and be alive), having adequate blood sugar is extremely important. But, keeping our blood sugar up is a relatively constant battle, as our blood sugar is always dropping.

Our brains are always active and are therefore always using blood sugar, which causes our blood sugar to drop slowly over time. And, when our brains or other parts of our bodies (such as muscles or organs) are highly active, like when we’re mentally or physically active, our blood sugar drops much faster.

If our blood sugar falls too low, our brains won’t have enough fuel and will shut off. So, when our blood sugar falls, our bodies adapt.

This is where feeling “hangry” comes in. We may begin to feel hungry, irritable, angry, weak, hot, nervous, anxious, jittery, or clammy (3). We also lack willpower and the ability to think as effectively (4, 5).

These effects are due to a lack of energy and are meant to reduce our blood sugar usage while also encouraging us to eat, which would raise our blood sugar. At the same time, low blood sugar activates our stress systems.

Blood Sugar and Stress

When our blood sugar drops too low, it doesn’t supply enough energy to our brains, resulting in stress. So, there are stress-induced mechanisms in place to raise our blood sugar.

The stress hormones glucagon, epinephrine (adrenaline), and growth hormone are released first (6). These hormones lead to glucose production by breaking down liver glycogen, the body’s stored form of sugar. They also switch the body’s primary fuel from sugar to fat in an effort to conserve sugar for our brains.

If these stress hormones can’t raise the blood sugar enough by breaking down liver glycogen (either because there isn’t enough glycogen or because energy is being used too quickly), then the stress hormone cortisol is released (6).

Cortisol breaks down protein, such as from muscles, organs, or other tissues, so that it can be converted to glucose through a process called gluconeogenesis. This is the last resort to raise blood sugar and supply energy.

Simply put, stress occurs when we don’t have enough energy, and then increases energy production via stress hormones. This may not sound like a big deal, but energy is integral to our health, and a lack of energy can be quite damaging.

This is evidenced by the fact that the stress hormones glucagon and cortisol are implicated in diabetes (7, 8) and that cortisol is strongly immunosuppressive and is implicated in obesity, heart disease, osteoporosis, depression and many other chronic diseases (9, 10, 11, 12).

The relationship between stress and health is acknowledged by the mainstream health community, but the relationship between blood sugar, stress, and health is not. And it’s an important one.

Blood sugar levels have an inverse relationship with stress, which makes sense considering blood sugar is an indirect measure of available energy (13, 14).

A higher blood sugar level allows us to handle greater amounts of stressors without causing stress. This relationship is so powerful that in rats with low blood sugar, certain toxins cause severe anaphylactic shock and death, while the same toxins cause only mild symptoms in rats protected by high blood sugar (16).

And, consuming carbohydrates that increase the blood sugar reduces stress that’s already occurring (14).

So, maintaining a higher, stable blood sugar will supply our brains (and the rest of our bodies) with the energy they need while inhibiting stress and the damage that comes with it.

Blood Sugar Confusion

Much of the confusion surrounding blood sugar comes from observations in people with insulin resistance or diabetes. In these cases, high blood sugar is common and is therefore blamed for some of the damage that goes on.

But, the problem in these conditions isn’t that the blood sugar is high, it’s that sugar isn’t able to be used to produce energy in the cells. Because sugar isn’t being used to produce energy, it builds up in the blood.

In these cases, the body is always under stress because it isn’t efficiently producing energy, which explains the elevated levels of glucagon and cortisol despite high blood sugar (7817).

(Note: When the ability to produce energy using sugar is inhibited or stress is already occurring, there’s no longer an inverse relationship between blood sugar and stress.)

(If you want to learn more about what actually causes type 2 diabetes and insulin resistance, check out this video.)

How to Maintain Stable Blood Sugar Levels

Maintaining a higher, stable blood sugar level supplies our bodies with the energy they need while inhibiting stress. This means improving fat loss and virtually all chronic diseases, while also preventing “hangriness.” Here are a few simple tips to help maintain a higher, stable blood sugar level throughout the day:

  • Our blood sugar is increased by carbohydrates, so eating carbohydrates allows us to maintain a higher blood sugar level and inhibits stress.
  • Our blood sugar decreases throughout the day, even at rest, and decreases even quicker when we’re physically or mentally active. So, eating a carbohydrate-containing snack or meal every 2-3 hours and after or during physical or mental activity will prevent blood sugar lows and stress.
  • Protein decreases blood sugar, so eating protein alone will cause our blood sugar to drop and stress to occur (18). But, this is easily preventable by making sure to eat carbohydrates anytime we eat protein.
References

Blood Sugar, Stress, and Feeling Hangry

“You’re not you when you’re hungry.”

I don’t know how well it sells candy bars, but I do know that it’s true, and a candy bar would probably help.

The word “hangry” has become popular lately and illustrates this idea pretty well. For those who don’t know, it’s a combination of the words “hungry” and “angry,” used to describe the feeling of irritability that we get when we’re hungry.

These feelings are actually symptoms of hypoglycemia, or low blood sugar. While the idea of feeling “hangry” has been getting more publicity, the importance of blood sugar in health is still largely overlooked, at least for those who don’t have diabetes.

Like the blaming of cholesterol for heart disease, the high blood sugar seen in insulin resistance and diabetes has been mistakenly blamed as a cause of the disease, as opposed to an effect. This has led to misconceptions surrounding blood sugar, including the ideas that “high blood sugar makes people fat and causes diabetes,” “eating protein stabilizes blood sugar levels,” and “sugar is unhealthy because it raises blood sugar.

On the contrary, maintaining a higher blood sugar, or rather, avoiding low blood sugar, is important for reducing stress and plays a major role in our health. Like many other misunderstood topics, this becomes clear when we consider how blood sugar relates to energy.

Blood Sugar and Energy

Energy allows every one of our cells to function. And, to produce energy, all our cells require fuel.

While most of the cells in the human body can use either carbohydrates or fat for fuel, the cells in our brain are unique. Our brain is the most energy-intensive of all our organs, and therefore requires fuel that produces the most energy in the most efficient manner: sugar (1, 2).

Sugar, or glucose, is transported throughout our bodies and to our brains by our blood. Our blood sugar is therefore an indicator of the amount of fuel we have available, or the amount of immediate energy our bodies can produce.

If our blood sugar is high, then our bodies have a lot of fuel available. And if our blood sugar is low, then our bodies don’t have very much fuel available.

Because our brains require sugar, and we need our brains to work in order to function (and be alive), having adequate blood sugar is extremely important. But, keeping our blood sugar up is a relatively constant battle, as our blood sugar is always dropping.

Our brains are always active and are therefore always using blood sugar, which causes our blood sugar to drop slowly over time. And, when our brains or other parts of our bodies (such as muscles or organs) are highly active, like when we’re mentally or physically active, our blood sugar drops much faster.

If our blood sugar falls too low, our brains won’t have enough fuel and will shut off. So, when our blood sugar falls, our bodies adapt.

This is where feeling “hangry” comes in. We may begin to feel hungry, irritable, angry, weak, hot, nervous, anxious, jittery, or clammy (3). We also lack willpower and the ability to think as effectively (4, 5).

These effects are due to a lack of energy and are meant to reduce our blood sugar usage while also encouraging us to eat, which would raise our blood sugar. At the same time, low blood sugar activates our stress systems.

Blood Sugar and Stress

When our blood sugar drops too low, it doesn’t supply enough energy to our brains, resulting in stress. So, there are stress-induced mechanisms in place to raise our blood sugar.

The stress hormones glucagon, epinephrine (adrenaline), and growth hormone are released first (6). These hormones lead to glucose production by breaking down liver glycogen, the body’s stored form of sugar. They also switch the body’s primary fuel from sugar to fat in an effort to conserve sugar for our brains.

If these stress hormones can’t raise the blood sugar enough by breaking down liver glycogen (either because there isn’t enough glycogen or because energy is being used too quickly), then the stress hormone cortisol is released (6).

Cortisol breaks down protein, such as from muscles, organs, or other tissues, so that it can be converted to glucose through a process called gluconeogenesis. This is the last resort to raise blood sugar and supply energy.

Simply put, stress occurs when we don’t have enough energy, and then increases energy production via stress hormones. This may not sound like a big deal, but energy is integral to our health, and a lack of energy can be quite damaging.

This is evidenced by the fact that the stress hormones glucagon and cortisol are implicated in diabetes (7, 8) and that cortisol is strongly immunosuppressive and is implicated in obesity, heart disease, osteoporosis, depression and many other chronic diseases (9, 10, 11, 12).

The relationship between stress and health is acknowledged by the mainstream health community, but the relationship between blood sugar, stress, and health is not. And it’s an important one.

Blood sugar levels have an inverse relationship with stress, which makes sense considering blood sugar is an indirect measure of available energy (13, 14).

A higher blood sugar level allows us to handle greater amounts of stressors without causing stress. This relationship is so powerful that in rats with low blood sugar, certain toxins cause severe anaphylactic shock and death, while the same toxins cause only mild symptoms in rats protected by high blood sugar (16).

And, consuming carbohydrates that increase the blood sugar reduces stress that’s already occurring (14).

So, maintaining a higher, stable blood sugar will supply our brains (and the rest of our bodies) with the energy they need while inhibiting stress and the damage that comes with it.

Blood Sugar Confusion

Much of the confusion surrounding blood sugar comes from observations in people with insulin resistance or diabetes. In these cases, high blood sugar is common and is therefore blamed for some of the damage that goes on.

But, the problem in these conditions isn’t that the blood sugar is high, it’s that sugar isn’t able to be used to produce energy in the cells. Because sugar isn’t being used to produce energy, it builds up in the blood.

In these cases, the body is always under stress because it isn’t efficiently producing energy, which explains the elevated levels of glucagon and cortisol despite high blood sugar (7817).

(Note: When the ability to produce energy using sugar is inhibited or stress is already occurring, there’s no longer an inverse relationship between blood sugar and stress.)

(If you want to learn more about what actually causes type 2 diabetes and insulin resistance, check out this video.)

How to Maintain Stable Blood Sugar Levels

Maintaining a higher, stable blood sugar level supplies our bodies with the energy they need while inhibiting stress. This means improving fat loss and virtually all chronic diseases, while also preventing “hangriness.” Here are a few simple tips to help maintain a higher, stable blood sugar level throughout the day:

  • Our blood sugar is increased by carbohydrates, so eating carbohydrates allows us to maintain a higher blood sugar level and inhibits stress.
  • Our blood sugar decreases throughout the day, even at rest, and decreases even quicker when we’re physically or mentally active. So, eating a carbohydrate-containing snack or meal every 2-3 hours and after or during physical or mental activity will prevent blood sugar lows and stress.
  • Protein decreases blood sugar, so eating protein alone will cause our blood sugar to drop and stress to occur (18). But, this is easily preventable by making sure to eat carbohydrates anytime we eat protein.
References

Blood Sugar, Stress, and Feeling Hangry

“You’re not you when you’re hungry.”

I don’t know how well it sells candy bars, but I do know that it’s true, and a candy bar would probably help.

The word “hangry” has become popular lately and illustrates this idea pretty well. For those who don’t know, it’s a combination of the words “hungry” and “angry,” used to describe the feeling of irritability that we get when we’re hungry.

These feelings are actually symptoms of hypoglycemia, or low blood sugar. While the idea of feeling “hangry” has been getting more publicity, the importance of blood sugar in health is still largely overlooked, at least for those who don’t have diabetes.

Like the blaming of cholesterol for heart disease, the high blood sugar seen in insulin resistance and diabetes has been mistakenly blamed as a cause of the disease, as opposed to an effect. This has led to misconceptions surrounding blood sugar, including the ideas that “high blood sugar makes people fat and causes diabetes,” “eating protein stabilizes blood sugar levels,” and “sugar is unhealthy because it raises blood sugar.

On the contrary, maintaining a higher blood sugar, or rather, avoiding low blood sugar, is important for reducing stress and plays a major role in our health. Like many other misunderstood topics, this becomes clear when we consider how blood sugar relates to energy.

Blood Sugar and Energy

Energy allows every one of our cells to function. And, to produce energy, all our cells require fuel.

While most of the cells in the human body can use either carbohydrates or fat for fuel, the cells in our brain are unique. Our brain is the most energy-intensive of all our organs, and therefore requires fuel that produces the most energy in the most efficient manner: sugar (1, 2).

Sugar, or glucose, is transported throughout our bodies and to our brains by our blood. Our blood sugar is therefore an indicator of the amount of fuel we have available, or the amount of immediate energy our bodies can produce.

If our blood sugar is high, then our bodies have a lot of fuel available. And if our blood sugar is low, then our bodies don’t have very much fuel available.

Because our brains require sugar, and we need our brains to work in order to function (and be alive), having adequate blood sugar is extremely important. But, keeping our blood sugar up is a relatively constant battle, as our blood sugar is always dropping.

Our brains are always active and are therefore always using blood sugar, which causes our blood sugar to drop slowly over time. And, when our brains or other parts of our bodies (such as muscles or organs) are highly active, like when we’re mentally or physically active, our blood sugar drops much faster.

If our blood sugar falls too low, our brains won’t have enough fuel and will shut off. So, when our blood sugar falls, our bodies adapt.

This is where feeling “hangry” comes in. We may begin to feel hungry, irritable, angry, weak, hot, nervous, anxious, jittery, or clammy (3). We also lack willpower and the ability to think as effectively (4, 5).

These effects are due to a lack of energy and are meant to reduce our blood sugar usage while also encouraging us to eat, which would raise our blood sugar. At the same time, low blood sugar activates our stress systems.

Blood Sugar and Stress

When our blood sugar drops too low, it doesn’t supply enough energy to our brains, resulting in stress. So, there are stress-induced mechanisms in place to raise our blood sugar.

The stress hormones glucagon, epinephrine (adrenaline), and growth hormone are released first (6). These hormones lead to glucose production by breaking down liver glycogen, the body’s stored form of sugar. They also switch the body’s primary fuel from sugar to fat in an effort to conserve sugar for our brains.

If these stress hormones can’t raise the blood sugar enough by breaking down liver glycogen (either because there isn’t enough glycogen or because energy is being used too quickly), then the stress hormone cortisol is released (6).

Cortisol breaks down protein, such as from muscles, organs, or other tissues, so that it can be converted to glucose through a process called gluconeogenesis. This is the last resort to raise blood sugar and supply energy.

Simply put, stress occurs when we don’t have enough energy, and then increases energy production via stress hormones. This may not sound like a big deal, but energy is integral to our health, and a lack of energy can be quite damaging.

This is evidenced by the fact that the stress hormones glucagon and cortisol are implicated in diabetes (7, 8) and that cortisol is strongly immunosuppressive and is implicated in obesity, heart disease, osteoporosis, depression and many other chronic diseases (9, 10, 11, 12).

The relationship between stress and health is acknowledged by the mainstream health community, but the relationship between blood sugar, stress, and health is not. And it’s an important one.

Blood sugar levels have an inverse relationship with stress, which makes sense considering blood sugar is an indirect measure of available energy (13, 14).

A higher blood sugar level allows us to handle greater amounts of stressors without causing stress. This relationship is so powerful that in rats with low blood sugar, certain toxins cause severe anaphylactic shock and death, while the same toxins cause only mild symptoms in rats protected by high blood sugar (16).

And, consuming carbohydrates that increase the blood sugar reduces stress that’s already occurring (14).

So, maintaining a higher, stable blood sugar will supply our brains (and the rest of our bodies) with the energy they need while inhibiting stress and the damage that comes with it.

Blood Sugar Confusion

Much of the confusion surrounding blood sugar comes from observations in people with insulin resistance or diabetes. In these cases, high blood sugar is common and is therefore blamed for some of the damage that goes on.

But, the problem in these conditions isn’t that the blood sugar is high, it’s that sugar isn’t able to be used to produce energy in the cells. Because sugar isn’t being used to produce energy, it builds up in the blood.

In these cases, the body is always under stress because it isn’t efficiently producing energy, which explains the elevated levels of glucagon and cortisol despite high blood sugar (7817).

(Note: When the ability to produce energy using sugar is inhibited or stress is already occurring, there’s no longer an inverse relationship between blood sugar and stress.)

(If you want to learn more about what actually causes type 2 diabetes and insulin resistance, check out this video.)

How to Maintain Stable Blood Sugar Levels

Maintaining a higher, stable blood sugar level supplies our bodies with the energy they need while inhibiting stress. This means improving fat loss and virtually all chronic diseases, while also preventing “hangriness.” Here are a few simple tips to help maintain a higher, stable blood sugar level throughout the day:

  • Our blood sugar is increased by carbohydrates, so eating carbohydrates allows us to maintain a higher blood sugar level and inhibits stress.
  • Our blood sugar decreases throughout the day, even at rest, and decreases even quicker when we’re physically or mentally active. So, eating a carbohydrate-containing snack or meal every 2-3 hours and after or during physical or mental activity will prevent blood sugar lows and stress.
  • Protein decreases blood sugar, so eating protein alone will cause our blood sugar to drop and stress to occur (18). But, this is easily preventable by making sure to eat carbohydrates anytime we eat protein.
References

Blood Sugar, Stress, and Feeling Hangry

“You’re not you when you’re hungry.”

I don’t know how well it sells candy bars, but I do know that it’s true, and a candy bar would probably help.

The word “hangry” has become popular lately and illustrates this idea pretty well. For those who don’t know, it’s a combination of the words “hungry” and “angry,” used to describe the feeling of irritability that we get when we’re hungry.

These feelings are actually symptoms of hypoglycemia, or low blood sugar. While the idea of feeling “hangry” has been getting more publicity, the importance of blood sugar in health is still largely overlooked, at least for those who don’t have diabetes.

Like the blaming of cholesterol for heart disease, the high blood sugar seen in insulin resistance and diabetes has been mistakenly blamed as a cause of the disease, as opposed to an effect. This has led to misconceptions surrounding blood sugar, including the ideas that “high blood sugar makes people fat and causes diabetes,” “eating protein stabilizes blood sugar levels,” and “sugar is unhealthy because it raises blood sugar.

On the contrary, maintaining a higher blood sugar, or rather, avoiding low blood sugar, is important for reducing stress and plays a major role in our health. Like many other misunderstood topics, this becomes clear when we consider how blood sugar relates to energy.

Blood Sugar and Energy

Energy allows every one of our cells to function. And, to produce energy, all our cells require fuel.

While most of the cells in the human body can use either carbohydrates or fat for fuel, the cells in our brain are unique. Our brain is the most energy-intensive of all our organs, and therefore requires fuel that produces the most energy in the most efficient manner: sugar (1, 2).

Sugar, or glucose, is transported throughout our bodies and to our brains by our blood. Our blood sugar is therefore an indicator of the amount of fuel we have available, or the amount of immediate energy our bodies can produce.

If our blood sugar is high, then our bodies have a lot of fuel available. And if our blood sugar is low, then our bodies don’t have very much fuel available.

Because our brains require sugar, and we need our brains to work in order to function (and be alive), having adequate blood sugar is extremely important. But, keeping our blood sugar up is a relatively constant battle, as our blood sugar is always dropping.

Our brains are always active and are therefore always using blood sugar, which causes our blood sugar to drop slowly over time. And, when our brains or other parts of our bodies (such as muscles or organs) are highly active, like when we’re mentally or physically active, our blood sugar drops much faster.

If our blood sugar falls too low, our brains won’t have enough fuel and will shut off. So, when our blood sugar falls, our bodies adapt.

This is where feeling “hangry” comes in. We may begin to feel hungry, irritable, angry, weak, hot, nervous, anxious, jittery, or clammy (3). We also lack willpower and the ability to think as effectively (4, 5).

These effects are due to a lack of energy and are meant to reduce our blood sugar usage while also encouraging us to eat, which would raise our blood sugar. At the same time, low blood sugar activates our stress systems.

Blood Sugar and Stress

When our blood sugar drops too low, it doesn’t supply enough energy to our brains, resulting in stress. So, there are stress-induced mechanisms in place to raise our blood sugar.

The stress hormones glucagon, epinephrine (adrenaline), and growth hormone are released first (6). These hormones lead to glucose production by breaking down liver glycogen, the body’s stored form of sugar. They also switch the body’s primary fuel from sugar to fat in an effort to conserve sugar for our brains.

If these stress hormones can’t raise the blood sugar enough by breaking down liver glycogen (either because there isn’t enough glycogen or because energy is being used too quickly), then the stress hormone cortisol is released (6).

Cortisol breaks down protein, such as from muscles, organs, or other tissues, so that it can be converted to glucose through a process called gluconeogenesis. This is the last resort to raise blood sugar and supply energy.

Simply put, stress occurs when we don’t have enough energy, and then increases energy production via stress hormones. This may not sound like a big deal, but energy is integral to our health, and a lack of energy can be quite damaging.

This is evidenced by the fact that the stress hormones glucagon and cortisol are implicated in diabetes (7, 8) and that cortisol is strongly immunosuppressive and is implicated in obesity, heart disease, osteoporosis, depression and many other chronic diseases (9, 10, 11, 12).

The relationship between stress and health is acknowledged by the mainstream health community, but the relationship between blood sugar, stress, and health is not. And it’s an important one.

Blood sugar levels have an inverse relationship with stress, which makes sense considering blood sugar is an indirect measure of available energy (13, 14).

A higher blood sugar level allows us to handle greater amounts of stressors without causing stress. This relationship is so powerful that in rats with low blood sugar, certain toxins cause severe anaphylactic shock and death, while the same toxins cause only mild symptoms in rats protected by high blood sugar (16).

And, consuming carbohydrates that increase the blood sugar reduces stress that’s already occurring (14).

So, maintaining a higher, stable blood sugar will supply our brains (and the rest of our bodies) with the energy they need while inhibiting stress and the damage that comes with it.

Blood Sugar Confusion

Much of the confusion surrounding blood sugar comes from observations in people with insulin resistance or diabetes. In these cases, high blood sugar is common and is therefore blamed for some of the damage that goes on.

But, the problem in these conditions isn’t that the blood sugar is high, it’s that sugar isn’t able to be used to produce energy in the cells. Because sugar isn’t being used to produce energy, it builds up in the blood.

In these cases, the body is always under stress because it isn’t efficiently producing energy, which explains the elevated levels of glucagon and cortisol despite high blood sugar (7817).

(Note: When the ability to produce energy using sugar is inhibited or stress is already occurring, there’s no longer an inverse relationship between blood sugar and stress.)

(If you want to learn more about what actually causes type 2 diabetes and insulin resistance, check out this video.)

How to Maintain Stable Blood Sugar Levels

Maintaining a higher, stable blood sugar level supplies our bodies with the energy they need while inhibiting stress. This means improving fat loss and virtually all chronic diseases, while also preventing “hangriness.” Here are a few simple tips to help maintain a higher, stable blood sugar level throughout the day:

  • Our blood sugar is increased by carbohydrates, so eating carbohydrates allows us to maintain a higher blood sugar level and inhibits stress.
  • Our blood sugar decreases throughout the day, even at rest, and decreases even quicker when we’re physically or mentally active. So, eating a carbohydrate-containing snack or meal every 2-3 hours and after or during physical or mental activity will prevent blood sugar lows and stress.
  • Protein decreases blood sugar, so eating protein alone will cause our blood sugar to drop and stress to occur (18). But, this is easily preventable by making sure to eat carbohydrates anytime we eat protein.
References

Blood Sugar, Stress, and Feeling Hangry

“You’re not you when you’re hungry.”

I don’t know how well it sells candy bars, but I do know that it’s true, and a candy bar would probably help.

The word “hangry” has become popular lately and illustrates this idea pretty well. For those who don’t know, it’s a combination of the words “hungry” and “angry,” used to describe the feeling of irritability that we get when we’re hungry.

These feelings are actually symptoms of hypoglycemia, or low blood sugar. While the idea of feeling “hangry” has been getting more publicity, the importance of blood sugar in health is still largely overlooked, at least for those who don’t have diabetes.

Like the blaming of cholesterol for heart disease, the high blood sugar seen in insulin resistance and diabetes has been mistakenly blamed as a cause of the disease, as opposed to an effect. This has led to misconceptions surrounding blood sugar, including the ideas that “high blood sugar makes people fat and causes diabetes,” “eating protein stabilizes blood sugar levels,” and “sugar is unhealthy because it raises blood sugar.

On the contrary, maintaining a higher blood sugar, or rather, avoiding low blood sugar, is important for reducing stress and plays a major role in our health. Like many other misunderstood topics, this becomes clear when we consider how blood sugar relates to energy.

Blood Sugar and Energy

Energy allows every one of our cells to function. And, to produce energy, all our cells require fuel.

While most of the cells in the human body can use either carbohydrates or fat for fuel, the cells in our brain are unique. Our brain is the most energy-intensive of all our organs, and therefore requires fuel that produces the most energy in the most efficient manner: sugar (1, 2).

Sugar, or glucose, is transported throughout our bodies and to our brains by our blood. Our blood sugar is therefore an indicator of the amount of fuel we have available, or the amount of immediate energy our bodies can produce.

If our blood sugar is high, then our bodies have a lot of fuel available. And if our blood sugar is low, then our bodies don’t have very much fuel available.

Because our brains require sugar, and we need our brains to work in order to function (and be alive), having adequate blood sugar is extremely important. But, keeping our blood sugar up is a relatively constant battle, as our blood sugar is always dropping.

Our brains are always active and are therefore always using blood sugar, which causes our blood sugar to drop slowly over time. And, when our brains or other parts of our bodies (such as muscles or organs) are highly active, like when we’re mentally or physically active, our blood sugar drops much faster.

If our blood sugar falls too low, our brains won’t have enough fuel and will shut off. So, when our blood sugar falls, our bodies adapt.

This is where feeling “hangry” comes in. We may begin to feel hungry, irritable, angry, weak, hot, nervous, anxious, jittery, or clammy (3). We also lack willpower and the ability to think as effectively (4, 5).

These effects are due to a lack of energy and are meant to reduce our blood sugar usage while also encouraging us to eat, which would raise our blood sugar. At the same time, low blood sugar activates our stress systems.

Blood Sugar and Stress

When our blood sugar drops too low, it doesn’t supply enough energy to our brains, resulting in stress. So, there are stress-induced mechanisms in place to raise our blood sugar.

The stress hormones glucagon, epinephrine (adrenaline), and growth hormone are released first (6). These hormones lead to glucose production by breaking down liver glycogen, the body’s stored form of sugar. They also switch the body’s primary fuel from sugar to fat in an effort to conserve sugar for our brains.

If these stress hormones can’t raise the blood sugar enough by breaking down liver glycogen (either because there isn’t enough glycogen or because energy is being used too quickly), then the stress hormone cortisol is released (6).

Cortisol breaks down protein, such as from muscles, organs, or other tissues, so that it can be converted to glucose through a process called gluconeogenesis. This is the last resort to raise blood sugar and supply energy.

Simply put, stress occurs when we don’t have enough energy, and then increases energy production via stress hormones. This may not sound like a big deal, but energy is integral to our health, and a lack of energy can be quite damaging.

This is evidenced by the fact that the stress hormones glucagon and cortisol are implicated in diabetes (7, 8) and that cortisol is strongly immunosuppressive and is implicated in obesity, heart disease, osteoporosis, depression and many other chronic diseases (9, 10, 11, 12).

The relationship between stress and health is acknowledged by the mainstream health community, but the relationship between blood sugar, stress, and health is not. And it’s an important one.

Blood sugar levels have an inverse relationship with stress, which makes sense considering blood sugar is an indirect measure of available energy (13, 14).

A higher blood sugar level allows us to handle greater amounts of stressors without causing stress. This relationship is so powerful that in rats with low blood sugar, certain toxins cause severe anaphylactic shock and death, while the same toxins cause only mild symptoms in rats protected by high blood sugar (16).

And, consuming carbohydrates that increase the blood sugar reduces stress that’s already occurring (14).

So, maintaining a higher, stable blood sugar will supply our brains (and the rest of our bodies) with the energy they need while inhibiting stress and the damage that comes with it.

Blood Sugar Confusion

Much of the confusion surrounding blood sugar comes from observations in people with insulin resistance or diabetes. In these cases, high blood sugar is common and is therefore blamed for some of the damage that goes on.

But, the problem in these conditions isn’t that the blood sugar is high, it’s that sugar isn’t able to be used to produce energy in the cells. Because sugar isn’t being used to produce energy, it builds up in the blood.

In these cases, the body is always under stress because it isn’t efficiently producing energy, which explains the elevated levels of glucagon and cortisol despite high blood sugar (7817).

(Note: When the ability to produce energy using sugar is inhibited or stress is already occurring, there’s no longer an inverse relationship between blood sugar and stress.)

(If you want to learn more about what actually causes type 2 diabetes and insulin resistance, check out this video.)

How to Maintain Stable Blood Sugar Levels

Maintaining a higher, stable blood sugar level supplies our bodies with the energy they need while inhibiting stress. This means improving fat loss and virtually all chronic diseases, while also preventing “hangriness.” Here are a few simple tips to help maintain a higher, stable blood sugar level throughout the day:

  • Our blood sugar is increased by carbohydrates, so eating carbohydrates allows us to maintain a higher blood sugar level and inhibits stress.
  • Our blood sugar decreases throughout the day, even at rest, and decreases even quicker when we’re physically or mentally active. So, eating a carbohydrate-containing snack or meal every 2-3 hours and after or during physical or mental activity will prevent blood sugar lows and stress.
  • Protein decreases blood sugar, so eating protein alone will cause our blood sugar to drop and stress to occur (18). But, this is easily preventable by making sure to eat carbohydrates anytime we eat protein.
References

Blood Sugar, Stress, and Feeling Hangry

“You’re not you when you’re hungry.”

I don’t know how well it sells candy bars, but I do know that it’s true, and a candy bar would probably help.

The word “hangry” has become popular lately and illustrates this idea pretty well. For those who don’t know, it’s a combination of the words “hungry” and “angry,” used to describe the feeling of irritability that we get when we’re hungry.

These feelings are actually symptoms of hypoglycemia, or low blood sugar. While the idea of feeling “hangry” has been getting more publicity, the importance of blood sugar in health is still largely overlooked, at least for those who don’t have diabetes.

Like the blaming of cholesterol for heart disease, the high blood sugar seen in insulin resistance and diabetes has been mistakenly blamed as a cause of the disease, as opposed to an effect. This has led to misconceptions surrounding blood sugar, including the ideas that “high blood sugar makes people fat and causes diabetes,” “eating protein stabilizes blood sugar levels,” and “sugar is unhealthy because it raises blood sugar.

On the contrary, maintaining a higher blood sugar, or rather, avoiding low blood sugar, is important for reducing stress and plays a major role in our health. Like many other misunderstood topics, this becomes clear when we consider how blood sugar relates to energy.

Blood Sugar and Energy

Energy allows every one of our cells to function. And, to produce energy, all our cells require fuel.

While most of the cells in the human body can use either carbohydrates or fat for fuel, the cells in our brain are unique. Our brain is the most energy-intensive of all our organs, and therefore requires fuel that produces the most energy in the most efficient manner: sugar (1, 2).

Sugar, or glucose, is transported throughout our bodies and to our brains by our blood. Our blood sugar is therefore an indicator of the amount of fuel we have available, or the amount of immediate energy our bodies can produce.

If our blood sugar is high, then our bodies have a lot of fuel available. And if our blood sugar is low, then our bodies don’t have very much fuel available.

Because our brains require sugar, and we need our brains to work in order to function (and be alive), having adequate blood sugar is extremely important. But, keeping our blood sugar up is a relatively constant battle, as our blood sugar is always dropping.

Our brains are always active and are therefore always using blood sugar, which causes our blood sugar to drop slowly over time. And, when our brains or other parts of our bodies (such as muscles or organs) are highly active, like when we’re mentally or physically active, our blood sugar drops much faster.

If our blood sugar falls too low, our brains won’t have enough fuel and will shut off. So, when our blood sugar falls, our bodies adapt.

This is where feeling “hangry” comes in. We may begin to feel hungry, irritable, angry, weak, hot, nervous, anxious, jittery, or clammy (3). We also lack willpower and the ability to think as effectively (4, 5).

These effects are due to a lack of energy and are meant to reduce our blood sugar usage while also encouraging us to eat, which would raise our blood sugar. At the same time, low blood sugar activates our stress systems.

Blood Sugar and Stress

When our blood sugar drops too low, it doesn’t supply enough energy to our brains, resulting in stress. So, there are stress-induced mechanisms in place to raise our blood sugar.

The stress hormones glucagon, epinephrine (adrenaline), and growth hormone are released first (6). These hormones lead to glucose production by breaking down liver glycogen, the body’s stored form of sugar. They also switch the body’s primary fuel from sugar to fat in an effort to conserve sugar for our brains.

If these stress hormones can’t raise the blood sugar enough by breaking down liver glycogen (either because there isn’t enough glycogen or because energy is being used too quickly), then the stress hormone cortisol is released (6).

Cortisol breaks down protein, such as from muscles, organs, or other tissues, so that it can be converted to glucose through a process called gluconeogenesis. This is the last resort to raise blood sugar and supply energy.

Simply put, stress occurs when we don’t have enough energy, and then increases energy production via stress hormones. This may not sound like a big deal, but energy is integral to our health, and a lack of energy can be quite damaging.

This is evidenced by the fact that the stress hormones glucagon and cortisol are implicated in diabetes (7, 8) and that cortisol is strongly immunosuppressive and is implicated in obesity, heart disease, osteoporosis, depression and many other chronic diseases (9, 10, 11, 12).

The relationship between stress and health is acknowledged by the mainstream health community, but the relationship between blood sugar, stress, and health is not. And it’s an important one.

Blood sugar levels have an inverse relationship with stress, which makes sense considering blood sugar is an indirect measure of available energy (13, 14).

A higher blood sugar level allows us to handle greater amounts of stressors without causing stress. This relationship is so powerful that in rats with low blood sugar, certain toxins cause severe anaphylactic shock and death, while the same toxins cause only mild symptoms in rats protected by high blood sugar (16).

And, consuming carbohydrates that increase the blood sugar reduces stress that’s already occurring (14).

So, maintaining a higher, stable blood sugar will supply our brains (and the rest of our bodies) with the energy they need while inhibiting stress and the damage that comes with it.

Blood Sugar Confusion

Much of the confusion surrounding blood sugar comes from observations in people with insulin resistance or diabetes. In these cases, high blood sugar is common and is therefore blamed for some of the damage that goes on.

But, the problem in these conditions isn’t that the blood sugar is high, it’s that sugar isn’t able to be used to produce energy in the cells. Because sugar isn’t being used to produce energy, it builds up in the blood.

In these cases, the body is always under stress because it isn’t efficiently producing energy, which explains the elevated levels of glucagon and cortisol despite high blood sugar (7817).

(Note: When the ability to produce energy using sugar is inhibited or stress is already occurring, there’s no longer an inverse relationship between blood sugar and stress.)

(If you want to learn more about what actually causes type 2 diabetes and insulin resistance, check out this video.)

How to Maintain Stable Blood Sugar Levels

Maintaining a higher, stable blood sugar level supplies our bodies with the energy they need while inhibiting stress. This means improving fat loss and virtually all chronic diseases, while also preventing “hangriness.” Here are a few simple tips to help maintain a higher, stable blood sugar level throughout the day:

  • Our blood sugar is increased by carbohydrates, so eating carbohydrates allows us to maintain a higher blood sugar level and inhibits stress.
  • Our blood sugar decreases throughout the day, even at rest, and decreases even quicker when we’re physically or mentally active. So, eating a carbohydrate-containing snack or meal every 2-3 hours and after or during physical or mental activity will prevent blood sugar lows and stress.
  • Protein decreases blood sugar, so eating protein alone will cause our blood sugar to drop and stress to occur (18). But, this is easily preventable by making sure to eat carbohydrates anytime we eat protein.
References

Blood Sugar, Stress, and Feeling Hangry

“You’re not you when you’re hungry.”

I don’t know how well it sells candy bars, but I do know that it’s true, and a candy bar would probably help.

The word “hangry” has become popular lately and illustrates this idea pretty well. For those who don’t know, it’s a combination of the words “hungry” and “angry,” used to describe the feeling of irritability that we get when we’re hungry.

These feelings are actually symptoms of hypoglycemia, or low blood sugar. While the idea of feeling “hangry” has been getting more publicity, the importance of blood sugar in health is still largely overlooked, at least for those who don’t have diabetes.

Like the blaming of cholesterol for heart disease, the high blood sugar seen in insulin resistance and diabetes has been mistakenly blamed as a cause of the disease, as opposed to an effect. This has led to misconceptions surrounding blood sugar, including the ideas that “high blood sugar makes people fat and causes diabetes,” “eating protein stabilizes blood sugar levels,” and “sugar is unhealthy because it raises blood sugar.

On the contrary, maintaining a higher blood sugar, or rather, avoiding low blood sugar, is important for reducing stress and plays a major role in our health. Like many other misunderstood topics, this becomes clear when we consider how blood sugar relates to energy.

Blood Sugar and Energy

Energy allows every one of our cells to function. And, to produce energy, all our cells require fuel.

While most of the cells in the human body can use either carbohydrates or fat for fuel, the cells in our brain are unique. Our brain is the most energy-intensive of all our organs, and therefore requires fuel that produces the most energy in the most efficient manner: sugar (1, 2).

Sugar, or glucose, is transported throughout our bodies and to our brains by our blood. Our blood sugar is therefore an indicator of the amount of fuel we have available, or the amount of immediate energy our bodies can produce.

If our blood sugar is high, then our bodies have a lot of fuel available. And if our blood sugar is low, then our bodies don’t have very much fuel available.

Because our brains require sugar, and we need our brains to work in order to function (and be alive), having adequate blood sugar is extremely important. But, keeping our blood sugar up is a relatively constant battle, as our blood sugar is always dropping.

Our brains are always active and are therefore always using blood sugar, which causes our blood sugar to drop slowly over time. And, when our brains or other parts of our bodies (such as muscles or organs) are highly active, like when we’re mentally or physically active, our blood sugar drops much faster.

If our blood sugar falls too low, our brains won’t have enough fuel and will shut off. So, when our blood sugar falls, our bodies adapt.

This is where feeling “hangry” comes in. We may begin to feel hungry, irritable, angry, weak, hot, nervous, anxious, jittery, or clammy (3). We also lack willpower and the ability to think as effectively (4, 5).

These effects are due to a lack of energy and are meant to reduce our blood sugar usage while also encouraging us to eat, which would raise our blood sugar. At the same time, low blood sugar activates our stress systems.

Blood Sugar and Stress

When our blood sugar drops too low, it doesn’t supply enough energy to our brains, resulting in stress. So, there are stress-induced mechanisms in place to raise our blood sugar.

The stress hormones glucagon, epinephrine (adrenaline), and growth hormone are released first (6). These hormones lead to glucose production by breaking down liver glycogen, the body’s stored form of sugar. They also switch the body’s primary fuel from sugar to fat in an effort to conserve sugar for our brains.

If these stress hormones can’t raise the blood sugar enough by breaking down liver glycogen (either because there isn’t enough glycogen or because energy is being used too quickly), then the stress hormone cortisol is released (6).

Cortisol breaks down protein, such as from muscles, organs, or other tissues, so that it can be converted to glucose through a process called gluconeogenesis. This is the last resort to raise blood sugar and supply energy.

Simply put, stress occurs when we don’t have enough energy, and then increases energy production via stress hormones. This may not sound like a big deal, but energy is integral to our health, and a lack of energy can be quite damaging.

This is evidenced by the fact that the stress hormones glucagon and cortisol are implicated in diabetes (7, 8) and that cortisol is strongly immunosuppressive and is implicated in obesity, heart disease, osteoporosis, depression and many other chronic diseases (9, 10, 11, 12).

The relationship between stress and health is acknowledged by the mainstream health community, but the relationship between blood sugar, stress, and health is not. And it’s an important one.

Blood sugar levels have an inverse relationship with stress, which makes sense considering blood sugar is an indirect measure of available energy (13, 14).

A higher blood sugar level allows us to handle greater amounts of stressors without causing stress. This relationship is so powerful that in rats with low blood sugar, certain toxins cause severe anaphylactic shock and death, while the same toxins cause only mild symptoms in rats protected by high blood sugar (16).

And, consuming carbohydrates that increase the blood sugar reduces stress that’s already occurring (14).

So, maintaining a higher, stable blood sugar will supply our brains (and the rest of our bodies) with the energy they need while inhibiting stress and the damage that comes with it.

Blood Sugar Confusion

Much of the confusion surrounding blood sugar comes from observations in people with insulin resistance or diabetes. In these cases, high blood sugar is common and is therefore blamed for some of the damage that goes on.

But, the problem in these conditions isn’t that the blood sugar is high, it’s that sugar isn’t able to be used to produce energy in the cells. Because sugar isn’t being used to produce energy, it builds up in the blood.

In these cases, the body is always under stress because it isn’t efficiently producing energy, which explains the elevated levels of glucagon and cortisol despite high blood sugar (7817).

(Note: When the ability to produce energy using sugar is inhibited or stress is already occurring, there’s no longer an inverse relationship between blood sugar and stress.)

(If you want to learn more about what actually causes type 2 diabetes and insulin resistance, check out this video.)

How to Maintain Stable Blood Sugar Levels

Maintaining a higher, stable blood sugar level supplies our bodies with the energy they need while inhibiting stress. This means improving fat loss and virtually all chronic diseases, while also preventing “hangriness.” Here are a few simple tips to help maintain a higher, stable blood sugar level throughout the day:

  • Our blood sugar is increased by carbohydrates, so eating carbohydrates allows us to maintain a higher blood sugar level and inhibits stress.
  • Our blood sugar decreases throughout the day, even at rest, and decreases even quicker when we’re physically or mentally active. So, eating a carbohydrate-containing snack or meal every 2-3 hours and after or during physical or mental activity will prevent blood sugar lows and stress.
  • Protein decreases blood sugar, so eating protein alone will cause our blood sugar to drop and stress to occur (18). But, this is easily preventable by making sure to eat carbohydrates anytime we eat protein.
References

Blood Sugar, Stress, and Feeling Hangry

“You’re not you when you’re hungry.”

I don’t know how well it sells candy bars, but I do know that it’s true, and a candy bar would probably help.

The word “hangry” has become popular lately and illustrates this idea pretty well. For those who don’t know, it’s a combination of the words “hungry” and “angry,” used to describe the feeling of irritability that we get when we’re hungry.

These feelings are actually symptoms of hypoglycemia, or low blood sugar. While the idea of feeling “hangry” has been getting more publicity, the importance of blood sugar in health is still largely overlooked, at least for those who don’t have diabetes.

Like the blaming of cholesterol for heart disease, the high blood sugar seen in insulin resistance and diabetes has been mistakenly blamed as a cause of the disease, as opposed to an effect. This has led to misconceptions surrounding blood sugar, including the ideas that “high blood sugar makes people fat and causes diabetes,” “eating protein stabilizes blood sugar levels,” and “sugar is unhealthy because it raises blood sugar.

On the contrary, maintaining a higher blood sugar, or rather, avoiding low blood sugar, is important for reducing stress and plays a major role in our health. Like many other misunderstood topics, this becomes clear when we consider how blood sugar relates to energy.

Blood Sugar and Energy

Energy allows every one of our cells to function. And, to produce energy, all our cells require fuel.

While most of the cells in the human body can use either carbohydrates or fat for fuel, the cells in our brain are unique. Our brain is the most energy-intensive of all our organs, and therefore requires fuel that produces the most energy in the most efficient manner: sugar (1, 2).

Sugar, or glucose, is transported throughout our bodies and to our brains by our blood. Our blood sugar is therefore an indicator of the amount of fuel we have available, or the amount of immediate energy our bodies can produce.

If our blood sugar is high, then our bodies have a lot of fuel available. And if our blood sugar is low, then our bodies don’t have very much fuel available.

Because our brains require sugar, and we need our brains to work in order to function (and be alive), having adequate blood sugar is extremely important. But, keeping our blood sugar up is a relatively constant battle, as our blood sugar is always dropping.

Our brains are always active and are therefore always using blood sugar, which causes our blood sugar to drop slowly over time. And, when our brains or other parts of our bodies (such as muscles or organs) are highly active, like when we’re mentally or physically active, our blood sugar drops much faster.

If our blood sugar falls too low, our brains won’t have enough fuel and will shut off. So, when our blood sugar falls, our bodies adapt.

This is where feeling “hangry” comes in. We may begin to feel hungry, irritable, angry, weak, hot, nervous, anxious, jittery, or clammy (3). We also lack willpower and the ability to think as effectively (4, 5).

These effects are due to a lack of energy and are meant to reduce our blood sugar usage while also encouraging us to eat, which would raise our blood sugar. At the same time, low blood sugar activates our stress systems.

Blood Sugar and Stress

When our blood sugar drops too low, it doesn’t supply enough energy to our brains, resulting in stress. So, there are stress-induced mechanisms in place to raise our blood sugar.

The stress hormones glucagon, epinephrine (adrenaline), and growth hormone are released first (6). These hormones lead to glucose production by breaking down liver glycogen, the body’s stored form of sugar. They also switch the body’s primary fuel from sugar to fat in an effort to conserve sugar for our brains.

If these stress hormones can’t raise the blood sugar enough by breaking down liver glycogen (either because there isn’t enough glycogen or because energy is being used too quickly), then the stress hormone cortisol is released (6).

Cortisol breaks down protein, such as from muscles, organs, or other tissues, so that it can be converted to glucose through a process called gluconeogenesis. This is the last resort to raise blood sugar and supply energy.

Simply put, stress occurs when we don’t have enough energy, and then increases energy production via stress hormones. This may not sound like a big deal, but energy is integral to our health, and a lack of energy can be quite damaging.

This is evidenced by the fact that the stress hormones glucagon and cortisol are implicated in diabetes (7, 8) and that cortisol is strongly immunosuppressive and is implicated in obesity, heart disease, osteoporosis, depression and many other chronic diseases (9, 10, 11, 12).

The relationship between stress and health is acknowledged by the mainstream health community, but the relationship between blood sugar, stress, and health is not. And it’s an important one.

Blood sugar levels have an inverse relationship with stress, which makes sense considering blood sugar is an indirect measure of available energy (13, 14).

A higher blood sugar level allows us to handle greater amounts of stressors without causing stress. This relationship is so powerful that in rats with low blood sugar, certain toxins cause severe anaphylactic shock and death, while the same toxins cause only mild symptoms in rats protected by high blood sugar (16).

And, consuming carbohydrates that increase the blood sugar reduces stress that’s already occurring (14).

So, maintaining a higher, stable blood sugar will supply our brains (and the rest of our bodies) with the energy they need while inhibiting stress and the damage that comes with it.

Blood Sugar Confusion

Much of the confusion surrounding blood sugar comes from observations in people with insulin resistance or diabetes. In these cases, high blood sugar is common and is therefore blamed for some of the damage that goes on.

But, the problem in these conditions isn’t that the blood sugar is high, it’s that sugar isn’t able to be used to produce energy in the cells. Because sugar isn’t being used to produce energy, it builds up in the blood.

In these cases, the body is always under stress because it isn’t efficiently producing energy, which explains the elevated levels of glucagon and cortisol despite high blood sugar (7817).

(Note: When the ability to produce energy using sugar is inhibited or stress is already occurring, there’s no longer an inverse relationship between blood sugar and stress.)

(If you want to learn more about what actually causes type 2 diabetes and insulin resistance, check out this video.)

How to Maintain Stable Blood Sugar Levels

Maintaining a higher, stable blood sugar level supplies our bodies with the energy they need while inhibiting stress. This means improving fat loss and virtually all chronic diseases, while also preventing “hangriness.” Here are a few simple tips to help maintain a higher, stable blood sugar level throughout the day:

  • Our blood sugar is increased by carbohydrates, so eating carbohydrates allows us to maintain a higher blood sugar level and inhibits stress.
  • Our blood sugar decreases throughout the day, even at rest, and decreases even quicker when we’re physically or mentally active. So, eating a carbohydrate-containing snack or meal every 2-3 hours and after or during physical or mental activity will prevent blood sugar lows and stress.
  • Protein decreases blood sugar, so eating protein alone will cause our blood sugar to drop and stress to occur (18). But, this is easily preventable by making sure to eat carbohydrates anytime we eat protein.
References

Blood Sugar, Stress, and Feeling Hangry

“You’re not you when you’re hungry.”

I don’t know how well it sells candy bars, but I do know that it’s true, and a candy bar would probably help.

The word “hangry” has become popular lately and illustrates this idea pretty well. For those who don’t know, it’s a combination of the words “hungry” and “angry,” used to describe the feeling of irritability that we get when we’re hungry.

These feelings are actually symptoms of hypoglycemia, or low blood sugar. While the idea of feeling “hangry” has been getting more publicity, the importance of blood sugar in health is still largely overlooked, at least for those who don’t have diabetes.

Like the blaming of cholesterol for heart disease, the high blood sugar seen in insulin resistance and diabetes has been mistakenly blamed as a cause of the disease, as opposed to an effect. This has led to misconceptions surrounding blood sugar, including the ideas that “high blood sugar makes people fat and causes diabetes,” “eating protein stabilizes blood sugar levels,” and “sugar is unhealthy because it raises blood sugar.

On the contrary, maintaining a higher blood sugar, or rather, avoiding low blood sugar, is important for reducing stress and plays a major role in our health. Like many other misunderstood topics, this becomes clear when we consider how blood sugar relates to energy.

Blood Sugar and Energy

Energy allows every one of our cells to function. And, to produce energy, all our cells require fuel.

While most of the cells in the human body can use either carbohydrates or fat for fuel, the cells in our brain are unique. Our brain is the most energy-intensive of all our organs, and therefore requires fuel that produces the most energy in the most efficient manner: sugar (1, 2).

Sugar, or glucose, is transported throughout our bodies and to our brains by our blood. Our blood sugar is therefore an indicator of the amount of fuel we have available, or the amount of immediate energy our bodies can produce.

If our blood sugar is high, then our bodies have a lot of fuel available. And if our blood sugar is low, then our bodies don’t have very much fuel available.

Because our brains require sugar, and we need our brains to work in order to function (and be alive), having adequate blood sugar is extremely important. But, keeping our blood sugar up is a relatively constant battle, as our blood sugar is always dropping.

Our brains are always active and are therefore always using blood sugar, which causes our blood sugar to drop slowly over time. And, when our brains or other parts of our bodies (such as muscles or organs) are highly active, like when we’re mentally or physically active, our blood sugar drops much faster.

If our blood sugar falls too low, our brains won’t have enough fuel and will shut off. So, when our blood sugar falls, our bodies adapt.

This is where feeling “hangry” comes in. We may begin to feel hungry, irritable, angry, weak, hot, nervous, anxious, jittery, or clammy (3). We also lack willpower and the ability to think as effectively (4, 5).

These effects are due to a lack of energy and are meant to reduce our blood sugar usage while also encouraging us to eat, which would raise our blood sugar. At the same time, low blood sugar activates our stress systems.

Blood Sugar and Stress

When our blood sugar drops too low, it doesn’t supply enough energy to our brains, resulting in stress. So, there are stress-induced mechanisms in place to raise our blood sugar.

The stress hormones glucagon, epinephrine (adrenaline), and growth hormone are released first (6). These hormones lead to glucose production by breaking down liver glycogen, the body’s stored form of sugar. They also switch the body’s primary fuel from sugar to fat in an effort to conserve sugar for our brains.

If these stress hormones can’t raise the blood sugar enough by breaking down liver glycogen (either because there isn’t enough glycogen or because energy is being used too quickly), then the stress hormone cortisol is released (6).

Cortisol breaks down protein, such as from muscles, organs, or other tissues, so that it can be converted to glucose through a process called gluconeogenesis. This is the last resort to raise blood sugar and supply energy.

Simply put, stress occurs when we don’t have enough energy, and then increases energy production via stress hormones. This may not sound like a big deal, but energy is integral to our health, and a lack of energy can be quite damaging.

This is evidenced by the fact that the stress hormones glucagon and cortisol are implicated in diabetes (7, 8) and that cortisol is strongly immunosuppressive and is implicated in obesity, heart disease, osteoporosis, depression and many other chronic diseases (9, 10, 11, 12).

The relationship between stress and health is acknowledged by the mainstream health community, but the relationship between blood sugar, stress, and health is not. And it’s an important one.

Blood sugar levels have an inverse relationship with stress, which makes sense considering blood sugar is an indirect measure of available energy (13, 14).

A higher blood sugar level allows us to handle greater amounts of stressors without causing stress. This relationship is so powerful that in rats with low blood sugar, certain toxins cause severe anaphylactic shock and death, while the same toxins cause only mild symptoms in rats protected by high blood sugar (16).

And, consuming carbohydrates that increase the blood sugar reduces stress that’s already occurring (14).

So, maintaining a higher, stable blood sugar will supply our brains (and the rest of our bodies) with the energy they need while inhibiting stress and the damage that comes with it.

Blood Sugar Confusion

Much of the confusion surrounding blood sugar comes from observations in people with insulin resistance or diabetes. In these cases, high blood sugar is common and is therefore blamed for some of the damage that goes on.

But, the problem in these conditions isn’t that the blood sugar is high, it’s that sugar isn’t able to be used to produce energy in the cells. Because sugar isn’t being used to produce energy, it builds up in the blood.

In these cases, the body is always under stress because it isn’t efficiently producing energy, which explains the elevated levels of glucagon and cortisol despite high blood sugar (7817).

(Note: When the ability to produce energy using sugar is inhibited or stress is already occurring, there’s no longer an inverse relationship between blood sugar and stress.)

(If you want to learn more about what actually causes type 2 diabetes and insulin resistance, check out this video.)

How to Maintain Stable Blood Sugar Levels

Maintaining a higher, stable blood sugar level supplies our bodies with the energy they need while inhibiting stress. This means improving fat loss and virtually all chronic diseases, while also preventing “hangriness.” Here are a few simple tips to help maintain a higher, stable blood sugar level throughout the day:

  • Our blood sugar is increased by carbohydrates, so eating carbohydrates allows us to maintain a higher blood sugar level and inhibits stress.
  • Our blood sugar decreases throughout the day, even at rest, and decreases even quicker when we’re physically or mentally active. So, eating a carbohydrate-containing snack or meal every 2-3 hours and after or during physical or mental activity will prevent blood sugar lows and stress.
  • Protein decreases blood sugar, so eating protein alone will cause our blood sugar to drop and stress to occur (18). But, this is easily preventable by making sure to eat carbohydrates anytime we eat protein.
References

Blood Sugar, Stress, and Feeling Hangry

“You’re not you when you’re hungry.”

I don’t know how well it sells candy bars, but I do know that it’s true, and a candy bar would probably help.

The word “hangry” has become popular lately and illustrates this idea pretty well. For those who don’t know, it’s a combination of the words “hungry” and “angry,” used to describe the feeling of irritability that we get when we’re hungry.

These feelings are actually symptoms of hypoglycemia, or low blood sugar. While the idea of feeling “hangry” has been getting more publicity, the importance of blood sugar in health is still largely overlooked, at least for those who don’t have diabetes.

Like the blaming of cholesterol for heart disease, the high blood sugar seen in insulin resistance and diabetes has been mistakenly blamed as a cause of the disease, as opposed to an effect. This has led to misconceptions surrounding blood sugar, including the ideas that “high blood sugar makes people fat and causes diabetes,” “eating protein stabilizes blood sugar levels,” and “sugar is unhealthy because it raises blood sugar.

On the contrary, maintaining a higher blood sugar, or rather, avoiding low blood sugar, is important for reducing stress and plays a major role in our health. Like many other misunderstood topics, this becomes clear when we consider how blood sugar relates to energy.

Blood Sugar and Energy

Energy allows every one of our cells to function. And, to produce energy, all our cells require fuel.

While most of the cells in the human body can use either carbohydrates or fat for fuel, the cells in our brain are unique. Our brain is the most energy-intensive of all our organs, and therefore requires fuel that produces the most energy in the most efficient manner: sugar (1, 2).

Sugar, or glucose, is transported throughout our bodies and to our brains by our blood. Our blood sugar is therefore an indicator of the amount of fuel we have available, or the amount of immediate energy our bodies can produce.

If our blood sugar is high, then our bodies have a lot of fuel available. And if our blood sugar is low, then our bodies don’t have very much fuel available.

Because our brains require sugar, and we need our brains to work in order to function (and be alive), having adequate blood sugar is extremely important. But, keeping our blood sugar up is a relatively constant battle, as our blood sugar is always dropping.

Our brains are always active and are therefore always using blood sugar, which causes our blood sugar to drop slowly over time. And, when our brains or other parts of our bodies (such as muscles or organs) are highly active, like when we’re mentally or physically active, our blood sugar drops much faster.

If our blood sugar falls too low, our brains won’t have enough fuel and will shut off. So, when our blood sugar falls, our bodies adapt.

This is where feeling “hangry” comes in. We may begin to feel hungry, irritable, angry, weak, hot, nervous, anxious, jittery, or clammy (3). We also lack willpower and the ability to think as effectively (4, 5).

These effects are due to a lack of energy and are meant to reduce our blood sugar usage while also encouraging us to eat, which would raise our blood sugar. At the same time, low blood sugar activates our stress systems.

Blood Sugar and Stress

When our blood sugar drops too low, it doesn’t supply enough energy to our brains, resulting in stress. So, there are stress-induced mechanisms in place to raise our blood sugar.

The stress hormones glucagon, epinephrine (adrenaline), and growth hormone are released first (6). These hormones lead to glucose production by breaking down liver glycogen, the body’s stored form of sugar. They also switch the body’s primary fuel from sugar to fat in an effort to conserve sugar for our brains.

If these stress hormones can’t raise the blood sugar enough by breaking down liver glycogen (either because there isn’t enough glycogen or because energy is being used too quickly), then the stress hormone cortisol is released (6).

Cortisol breaks down protein, such as from muscles, organs, or other tissues, so that it can be converted to glucose through a process called gluconeogenesis. This is the last resort to raise blood sugar and supply energy.

Simply put, stress occurs when we don’t have enough energy, and then increases energy production via stress hormones. This may not sound like a big deal, but energy is integral to our health, and a lack of energy can be quite damaging.

This is evidenced by the fact that the stress hormones glucagon and cortisol are implicated in diabetes (7, 8) and that cortisol is strongly immunosuppressive and is implicated in obesity, heart disease, osteoporosis, depression and many other chronic diseases (9, 10, 11, 12).

The relationship between stress and health is acknowledged by the mainstream health community, but the relationship between blood sugar, stress, and health is not. And it’s an important one.

Blood sugar levels have an inverse relationship with stress, which makes sense considering blood sugar is an indirect measure of available energy (13, 14).

A higher blood sugar level allows us to handle greater amounts of stressors without causing stress. This relationship is so powerful that in rats with low blood sugar, certain toxins cause severe anaphylactic shock and death, while the same toxins cause only mild symptoms in rats protected by high blood sugar (16).

And, consuming carbohydrates that increase the blood sugar reduces stress that’s already occurring (14).

So, maintaining a higher, stable blood sugar will supply our brains (and the rest of our bodies) with the energy they need while inhibiting stress and the damage that comes with it.

Blood Sugar Confusion

Much of the confusion surrounding blood sugar comes from observations in people with insulin resistance or diabetes. In these cases, high blood sugar is common and is therefore blamed for some of the damage that goes on.

But, the problem in these conditions isn’t that the blood sugar is high, it’s that sugar isn’t able to be used to produce energy in the cells. Because sugar isn’t being used to produce energy, it builds up in the blood.

In these cases, the body is always under stress because it isn’t efficiently producing energy, which explains the elevated levels of glucagon and cortisol despite high blood sugar (7817).

(Note: When the ability to produce energy using sugar is inhibited or stress is already occurring, there’s no longer an inverse relationship between blood sugar and stress.)

(If you want to learn more about what actually causes type 2 diabetes and insulin resistance, check out this video.)

How to Maintain Stable Blood Sugar Levels

Maintaining a higher, stable blood sugar level supplies our bodies with the energy they need while inhibiting stress. This means improving fat loss and virtually all chronic diseases, while also preventing “hangriness.” Here are a few simple tips to help maintain a higher, stable blood sugar level throughout the day:

  • Our blood sugar is increased by carbohydrates, so eating carbohydrates allows us to maintain a higher blood sugar level and inhibits stress.
  • Our blood sugar decreases throughout the day, even at rest, and decreases even quicker when we’re physically or mentally active. So, eating a carbohydrate-containing snack or meal every 2-3 hours and after or during physical or mental activity will prevent blood sugar lows and stress.
  • Protein decreases blood sugar, so eating protein alone will cause our blood sugar to drop and stress to occur (18). But, this is easily preventable by making sure to eat carbohydrates anytime we eat protein.
References

Blood Sugar, Stress, and Feeling Hangry

“You’re not you when you’re hungry.”

I don’t know how well it sells candy bars, but I do know that it’s true, and a candy bar would probably help.

The word “hangry” has become popular lately and illustrates this idea pretty well. For those who don’t know, it’s a combination of the words “hungry” and “angry,” used to describe the feeling of irritability that we get when we’re hungry.

These feelings are actually symptoms of hypoglycemia, or low blood sugar. While the idea of feeling “hangry” has been getting more publicity, the importance of blood sugar in health is still largely overlooked, at least for those who don’t have diabetes.

Like the blaming of cholesterol for heart disease, the high blood sugar seen in insulin resistance and diabetes has been mistakenly blamed as a cause of the disease, as opposed to an effect. This has led to misconceptions surrounding blood sugar, including the ideas that “high blood sugar makes people fat and causes diabetes,” “eating protein stabilizes blood sugar levels,” and “sugar is unhealthy because it raises blood sugar.

On the contrary, maintaining a higher blood sugar, or rather, avoiding low blood sugar, is important for reducing stress and plays a major role in our health. Like many other misunderstood topics, this becomes clear when we consider how blood sugar relates to energy.

Blood Sugar and Energy

Energy allows every one of our cells to function. And, to produce energy, all our cells require fuel.

While most of the cells in the human body can use either carbohydrates or fat for fuel, the cells in our brain are unique. Our brain is the most energy-intensive of all our organs, and therefore requires fuel that produces the most energy in the most efficient manner: sugar (1, 2).

Sugar, or glucose, is transported throughout our bodies and to our brains by our blood. Our blood sugar is therefore an indicator of the amount of fuel we have available, or the amount of immediate energy our bodies can produce.

If our blood sugar is high, then our bodies have a lot of fuel available. And if our blood sugar is low, then our bodies don’t have very much fuel available.

Because our brains require sugar, and we need our brains to work in order to function (and be alive), having adequate blood sugar is extremely important. But, keeping our blood sugar up is a relatively constant battle, as our blood sugar is always dropping.

Our brains are always active and are therefore always using blood sugar, which causes our blood sugar to drop slowly over time. And, when our brains or other parts of our bodies (such as muscles or organs) are highly active, like when we’re mentally or physically active, our blood sugar drops much faster.

If our blood sugar falls too low, our brains won’t have enough fuel and will shut off. So, when our blood sugar falls, our bodies adapt.

This is where feeling “hangry” comes in. We may begin to feel hungry, irritable, angry, weak, hot, nervous, anxious, jittery, or clammy (3). We also lack willpower and the ability to think as effectively (4, 5).

These effects are due to a lack of energy and are meant to reduce our blood sugar usage while also encouraging us to eat, which would raise our blood sugar. At the same time, low blood sugar activates our stress systems.

Blood Sugar and Stress

When our blood sugar drops too low, it doesn’t supply enough energy to our brains, resulting in stress. So, there are stress-induced mechanisms in place to raise our blood sugar.

The stress hormones glucagon, epinephrine (adrenaline), and growth hormone are released first (6). These hormones lead to glucose production by breaking down liver glycogen, the body’s stored form of sugar. They also switch the body’s primary fuel from sugar to fat in an effort to conserve sugar for our brains.

If these stress hormones can’t raise the blood sugar enough by breaking down liver glycogen (either because there isn’t enough glycogen or because energy is being used too quickly), then the stress hormone cortisol is released (6).

Cortisol breaks down protein, such as from muscles, organs, or other tissues, so that it can be converted to glucose through a process called gluconeogenesis. This is the last resort to raise blood sugar and supply energy.

Simply put, stress occurs when we don’t have enough energy, and then increases energy production via stress hormones. This may not sound like a big deal, but energy is integral to our health, and a lack of energy can be quite damaging.

This is evidenced by the fact that the stress hormones glucagon and cortisol are implicated in diabetes (7, 8) and that cortisol is strongly immunosuppressive and is implicated in obesity, heart disease, osteoporosis, depression and many other chronic diseases (9, 10, 11, 12).

The relationship between stress and health is acknowledged by the mainstream health community, but the relationship between blood sugar, stress, and health is not. And it’s an important one.

Blood sugar levels have an inverse relationship with stress, which makes sense considering blood sugar is an indirect measure of available energy (13, 14).

A higher blood sugar level allows us to handle greater amounts of stressors without causing stress. This relationship is so powerful that in rats with low blood sugar, certain toxins cause severe anaphylactic shock and death, while the same toxins cause only mild symptoms in rats protected by high blood sugar (16).

And, consuming carbohydrates that increase the blood sugar reduces stress that’s already occurring (14).

So, maintaining a higher, stable blood sugar will supply our brains (and the rest of our bodies) with the energy they need while inhibiting stress and the damage that comes with it.

Blood Sugar Confusion

Much of the confusion surrounding blood sugar comes from observations in people with insulin resistance or diabetes. In these cases, high blood sugar is common and is therefore blamed for some of the damage that goes on.

But, the problem in these conditions isn’t that the blood sugar is high, it’s that sugar isn’t able to be used to produce energy in the cells. Because sugar isn’t being used to produce energy, it builds up in the blood.

In these cases, the body is always under stress because it isn’t efficiently producing energy, which explains the elevated levels of glucagon and cortisol despite high blood sugar (7817).

(Note: When the ability to produce energy using sugar is inhibited or stress is already occurring, there’s no longer an inverse relationship between blood sugar and stress.)

(If you want to learn more about what actually causes type 2 diabetes and insulin resistance, check out this video.)

How to Maintain Stable Blood Sugar Levels

Maintaining a higher, stable blood sugar level supplies our bodies with the energy they need while inhibiting stress. This means improving fat loss and virtually all chronic diseases, while also preventing “hangriness.” Here are a few simple tips to help maintain a higher, stable blood sugar level throughout the day:

  • Our blood sugar is increased by carbohydrates, so eating carbohydrates allows us to maintain a higher blood sugar level and inhibits stress.
  • Our blood sugar decreases throughout the day, even at rest, and decreases even quicker when we’re physically or mentally active. So, eating a carbohydrate-containing snack or meal every 2-3 hours and after or during physical or mental activity will prevent blood sugar lows and stress.
  • Protein decreases blood sugar, so eating protein alone will cause our blood sugar to drop and stress to occur (18). But, this is easily preventable by making sure to eat carbohydrates anytime we eat protein.
References

Blood Sugar, Stress, and Feeling Hangry

“You’re not you when you’re hungry.”

I don’t know how well it sells candy bars, but I do know that it’s true, and a candy bar would probably help.

The word “hangry” has become popular lately and illustrates this idea pretty well. For those who don’t know, it’s a combination of the words “hungry” and “angry,” used to describe the feeling of irritability that we get when we’re hungry.

These feelings are actually symptoms of hypoglycemia, or low blood sugar. While the idea of feeling “hangry” has been getting more publicity, the importance of blood sugar in health is still largely overlooked, at least for those who don’t have diabetes.

Like the blaming of cholesterol for heart disease, the high blood sugar seen in insulin resistance and diabetes has been mistakenly blamed as a cause of the disease, as opposed to an effect. This has led to misconceptions surrounding blood sugar, including the ideas that “high blood sugar makes people fat and causes diabetes,” “eating protein stabilizes blood sugar levels,” and “sugar is unhealthy because it raises blood sugar.

On the contrary, maintaining a higher blood sugar, or rather, avoiding low blood sugar, is important for reducing stress and plays a major role in our health. Like many other misunderstood topics, this becomes clear when we consider how blood sugar relates to energy.

Blood Sugar and Energy

Energy allows every one of our cells to function. And, to produce energy, all our cells require fuel.

While most of the cells in the human body can use either carbohydrates or fat for fuel, the cells in our brain are unique. Our brain is the most energy-intensive of all our organs, and therefore requires fuel that produces the most energy in the most efficient manner: sugar (1, 2).

Sugar, or glucose, is transported throughout our bodies and to our brains by our blood. Our blood sugar is therefore an indicator of the amount of fuel we have available, or the amount of immediate energy our bodies can produce.

If our blood sugar is high, then our bodies have a lot of fuel available. And if our blood sugar is low, then our bodies don’t have very much fuel available.

Because our brains require sugar, and we need our brains to work in order to function (and be alive), having adequate blood sugar is extremely important. But, keeping our blood sugar up is a relatively constant battle, as our blood sugar is always dropping.

Our brains are always active and are therefore always using blood sugar, which causes our blood sugar to drop slowly over time. And, when our brains or other parts of our bodies (such as muscles or organs) are highly active, like when we’re mentally or physically active, our blood sugar drops much faster.

If our blood sugar falls too low, our brains won’t have enough fuel and will shut off. So, when our blood sugar falls, our bodies adapt.

This is where feeling “hangry” comes in. We may begin to feel hungry, irritable, angry, weak, hot, nervous, anxious, jittery, or clammy (3). We also lack willpower and the ability to think as effectively (4, 5).

These effects are due to a lack of energy and are meant to reduce our blood sugar usage while also encouraging us to eat, which would raise our blood sugar. At the same time, low blood sugar activates our stress systems.

Blood Sugar and Stress

When our blood sugar drops too low, it doesn’t supply enough energy to our brains, resulting in stress. So, there are stress-induced mechanisms in place to raise our blood sugar.

The stress hormones glucagon, epinephrine (adrenaline), and growth hormone are released first (6). These hormones lead to glucose production by breaking down liver glycogen, the body’s stored form of sugar. They also switch the body’s primary fuel from sugar to fat in an effort to conserve sugar for our brains.

If these stress hormones can’t raise the blood sugar enough by breaking down liver glycogen (either because there isn’t enough glycogen or because energy is being used too quickly), then the stress hormone cortisol is released (6).

Cortisol breaks down protein, such as from muscles, organs, or other tissues, so that it can be converted to glucose through a process called gluconeogenesis. This is the last resort to raise blood sugar and supply energy.

Simply put, stress occurs when we don’t have enough energy, and then increases energy production via stress hormones. This may not sound like a big deal, but energy is integral to our health, and a lack of energy can be quite damaging.

This is evidenced by the fact that the stress hormones glucagon and cortisol are implicated in diabetes (7, 8) and that cortisol is strongly immunosuppressive and is implicated in obesity, heart disease, osteoporosis, depression and many other chronic diseases (9, 10, 11, 12).

The relationship between stress and health is acknowledged by the mainstream health community, but the relationship between blood sugar, stress, and health is not. And it’s an important one.

Blood sugar levels have an inverse relationship with stress, which makes sense considering blood sugar is an indirect measure of available energy (13, 14).

A higher blood sugar level allows us to handle greater amounts of stressors without causing stress. This relationship is so powerful that in rats with low blood sugar, certain toxins cause severe anaphylactic shock and death, while the same toxins cause only mild symptoms in rats protected by high blood sugar (16).

And, consuming carbohydrates that increase the blood sugar reduces stress that’s already occurring (14).

So, maintaining a higher, stable blood sugar will supply our brains (and the rest of our bodies) with the energy they need while inhibiting stress and the damage that comes with it.

Blood Sugar Confusion

Much of the confusion surrounding blood sugar comes from observations in people with insulin resistance or diabetes. In these cases, high blood sugar is common and is therefore blamed for some of the damage that goes on.

But, the problem in these conditions isn’t that the blood sugar is high, it’s that sugar isn’t able to be used to produce energy in the cells. Because sugar isn’t being used to produce energy, it builds up in the blood.

In these cases, the body is always under stress because it isn’t efficiently producing energy, which explains the elevated levels of glucagon and cortisol despite high blood sugar (7817).

(Note: When the ability to produce energy using sugar is inhibited or stress is already occurring, there’s no longer an inverse relationship between blood sugar and stress.)

(If you want to learn more about what actually causes type 2 diabetes and insulin resistance, check out this video.)

How to Maintain Stable Blood Sugar Levels

Maintaining a higher, stable blood sugar level supplies our bodies with the energy they need while inhibiting stress. This means improving fat loss and virtually all chronic diseases, while also preventing “hangriness.” Here are a few simple tips to help maintain a higher, stable blood sugar level throughout the day:

  • Our blood sugar is increased by carbohydrates, so eating carbohydrates allows us to maintain a higher blood sugar level and inhibits stress.
  • Our blood sugar decreases throughout the day, even at rest, and decreases even quicker when we’re physically or mentally active. So, eating a carbohydrate-containing snack or meal every 2-3 hours and after or during physical or mental activity will prevent blood sugar lows and stress.
  • Protein decreases blood sugar, so eating protein alone will cause our blood sugar to drop and stress to occur (18). But, this is easily preventable by making sure to eat carbohydrates anytime we eat protein.
References

Grains and Legumes and Antinutrients, Oh My!

Despite the growing anti-grain movement, it’s still recommended that we consume 5-8 ounce equivalents or more of grains per day, and whole grains are still the face of the typical healthy diet (1).

Mainstream nutrition recommendations tell us that whole grains, pseudograins, and legumes are heart-healthy and promote a healthy weight. These food groups include foods like:

  • Wheat, corn, rye, barely, rice, millet, oats (grains)
  • Quinoa, amaranth, buckwheat (pseudograins)
  • Beans, soy, lentils, peanuts (legumes)

On the other hand, refined grains are the ones blamed for obesity, diabetes, and heart disease.

 

Holy Whole Grains vs. Evil Refined Grains

Let’s start with the basics.

Grains, pseudograins, and legumes are all seeds, which have 3 main components: bran, germ, and endosperm. The bran and germ contain most of the fiber and “nutrients,” and the endosperm is the carbohydrate-dense portion.

A whole grain is still intact – it contains all 3 of these components, while refined grains are stripped of the germ and bran, leaving only the endosperm.

So, the only difference between the “healthiest-of-all-foods” whole grains and the “inflammation-diabetes-obesity-and-heart-disease-causing” refined grains are the fiber and the “nutrients,” while the starch-containing endosperm is the same.

And, like whole grains, the “heart-healthy” pseudograins and legumes are full of fiber and “nutrients.”

But, it turns out that the fibers and “nutrients” found in these foods might not be so beneficial after all, leaving their supposed health-promoting effects in question.

 

Grains, Legumes, and Fiber

Whole grains, pseudograins, and legumes contain both soluble and insoluble fibers.

Soluble fibers are considered prebiotics because they feed our gut bacteria, whereas insoluble fibers are not digested by our gut bacteria and help to move food through our guts.

These fibers are considered beneficial because of ability to keep us full for longer, their prebiotic effects, and their colon cleansing effects.

But, these effects aren’t always so beneficial.

Keeping us full for longer might be favorable if we wanted to eat less, but eating less isn’t really beneficial unless we want to deprive ourselves of energy (Why “Eat Less and Exercise More” is the WORST Advice for Fat Loss and Health).

The ability for soluble fibers to feed our gut bacteria may sound healthy when it’s phrased as “feeding our good bacteria,” but this is more like wishful thinking. These fibers do feed our gut bacteria, but they feed the bad ones in addition to the good ones.

This isn’t a problem if our gut function and microbiome composition are optimal. But, if they aren’t optimal, which is extraordinarily common in modern times, this will exacerbate any gut dysfunction that’s going on.

(Fun fact: the gas that’s commonly associated with eating beans is a product of a suboptimal microbiome consuming soluble fiber)

On the other hand, the ability for insoluble fibers to move food through our gut is beneficial because gut motility is important for healthy gut function. But, this is a relatively trivial benefit in the context of grain consumption.

 

Grains, Legumes, and (Anti)nutrients

Whole grains, pseudograins, and legumes are touted for their nutrient content, specifically their vitamins, minerals, and protein. But when we consider their antinutrient content, their nutrient value is really pretty poor.

As I mentioned earlier, grains, pseudograins, and legumes are seeds. Seeds are an extraordinarily important part of plants – they’re needed for plants to reproduce. The nutrients in seeds aren’t meant for us, they’re meant to be used for growing a new plant.

Plants can’t protect their valuable seeds by running from predators or attacking them with sharp claws or teeth. Instead, their seeds have chemical defenses – compounds that protect their nutrients and cause harm to animals who eat them. These compounds are commonly referred to as antinutrients.

There are several types of antinutrients, including lectins, phytic acid (phytates), oxalic acid (oxalates), enzyme inhibitors, and saponins, each with unique harmful effects.

Lectins

Lectins are probably the most damaging and well-known antinutrients. You’ve probably heard of the most infamous lectin, gluten. Lectins inhibit nutrient absorption, cause bacterial overgrowth and systemic stress and inflammation, and damage our gut barrier, causing it to become permeable or “leaky” (2, 3, 4, 5, 6).

Gut permeability, or “leakiness,” allows undigested food particles and toxins to travel directly into the bloodstream, which can impair energy production and contribute to stress and inflammation (7, 8).

Phytic Acid and Oxalic Acid

Phytic acid and oxalic acid bind with calcium, magnesium, zinc, copper, potassium, iron, and other minerals, blocking their digestion and absorption in our guts and inhibiting our ability to use them (9, 10, 11). These minerals are vital for many processes, one of the most noteworthy being energy production.

Enzyme Inhibitors

Enzyme inhibitors block the enzymes in our guts that digest protein and starch, which prevents the digestion and absorption of protein and starches in the grains, pseudograins, and legumes, as well as in other foods we happen to be eating with them (9, 12, 13). Phytic acid also blocks some of these enzymes, further inhibiting the digestion of protein and starch (14, 15).

Saponins

Saponins, which are found mostly in pseudograins and legumes, inhibit protein-digesting enzymes, inhibit thyroid function (the regulator of our metabolism), and bind with and lower cholesterol (this isn’t beneficial, as we might be led to believe – I explain why here) (16, 17, 18).

 

Antinutrients No More

Somehow, the mainstream has found ways to spin the harmful effects of antinutrients into benefits. Impairing energy production and contributing to inflammation is considered “boosting immune function,” impairing starch digestion is considered “managing blood sugar,” and reducing cholesterol is, well, just reducing cholesterol, but this isn’t beneficial like we’ve been told.

If you ask me, it’s pretty clear that whole grains and legumes aren’t the health foods they’ve been made out to be. If anything, they appear to be worse than their obesity-, diabetes-, and heart disease-causing counterparts, refined grains. And this isn’t to mention the pesticides and GMOs that are ubiquitous among these crops.

But, it’s not all bad. In fact, grains and legumes can be prepared in ways that negate many of their negative effects. Cooking can deactivate a few of the antinutrients in these foods, but the traditional preparations of soaking, sprouting, and fermenting significantly reduce their antinutrient content, and may even alter their fiber composition (9, 19).

But if that doesn’t suit your fancy, you can skip these foods altogether!

Grains are most certainly not a necessary part of a healthy diet like they’ve been made out to be. Fruits and starch-containing foods that aren’t grains, including roots (carrots, yuca, turnips, etc.), tubers (potatoes and sweet potatoes), and vegetables in the gourd family (like squash and zucchini), are all great sources of carbohydrates with few antinutrients, if any.

(Note: some of these foods, like potatoes, do have antinutrients. But, they’re housed in the skins which can be easily removed.)

Also, while it is a grain, white rice is a relatively antinutrient-free carbohydrate source. This is because it’s stripped of its bran and hull, the parts of brown rice that contain most of the antinutrients.

Does all of this mean that if you eat any non-traditionally prepared grains, pseudograins, or legumes you can say goodbye to your health?

Of course not. But it does mean that their promotion as “health foods” is not supported, and we may want to reconsider how much of them we’re eating.

 

References

Grains and Legumes and Antinutrients, Oh My!

Despite the growing anti-grain movement, it’s still recommended that we consume 5-8 ounce equivalents or more of grains per day, and whole grains are still the face of the typical healthy diet (1).

Mainstream nutrition recommendations tell us that whole grains, pseudograins, and legumes are heart-healthy and promote a healthy weight. These food groups include foods like:

  • Wheat, corn, rye, barely, rice, millet, oats (grains)
  • Quinoa, amaranth, buckwheat (pseudograins)
  • Beans, soy, lentils, peanuts (legumes)

On the other hand, refined grains are the ones blamed for obesity, diabetes, and heart disease.

 

Holy Whole Grains vs. Evil Refined Grains

Let’s start with the basics.

Grains, pseudograins, and legumes are all seeds, which have 3 main components: bran, germ, and endosperm. The bran and germ contain most of the fiber and “nutrients,” and the endosperm is the carbohydrate-dense portion.

A whole grain is still intact – it contains all 3 of these components, while refined grains are stripped of the germ and bran, leaving only the endosperm.

So, the only difference between the “healthiest-of-all-foods” whole grains and the “inflammation-diabetes-obesity-and-heart-disease-causing” refined grains are the fiber and the “nutrients,” while the starch-containing endosperm is the same.

And, like whole grains, the “heart-healthy” pseudograins and legumes are full of fiber and “nutrients.”

But, it turns out that the fibers and “nutrients” found in these foods might not be so beneficial after all, leaving their supposed health-promoting effects in question.

 

Grains, Legumes, and Fiber

Whole grains, pseudograins, and legumes contain both soluble and insoluble fibers.

Soluble fibers are considered prebiotics because they feed our gut bacteria, whereas insoluble fibers are not digested by our gut bacteria and help to move food through our guts.

These fibers are considered beneficial because of ability to keep us full for longer, their prebiotic effects, and their colon cleansing effects.

But, these effects aren’t always so beneficial.

Keeping us full for longer might be favorable if we wanted to eat less, but eating less isn’t really beneficial unless we want to deprive ourselves of energy (Why “Eat Less and Exercise More” is the WORST Advice for Fat Loss and Health).

The ability for soluble fibers to feed our gut bacteria may sound healthy when it’s phrased as “feeding our good bacteria,” but this is more like wishful thinking. These fibers do feed our gut bacteria, but they feed the bad ones in addition to the good ones.

This isn’t a problem if our gut function and microbiome composition are optimal. But, if they aren’t optimal, which is extraordinarily common in modern times, this will exacerbate any gut dysfunction that’s going on.

(Fun fact: the gas that’s commonly associated with eating beans is a product of a suboptimal microbiome consuming soluble fiber)

On the other hand, the ability for insoluble fibers to move food through our gut is beneficial because gut motility is important for healthy gut function. But, this is a relatively trivial benefit in the context of grain consumption.

 

Grains, Legumes, and (Anti)nutrients

Whole grains, pseudograins, and legumes are touted for their nutrient content, specifically their vitamins, minerals, and protein. But when we consider their antinutrient content, their nutrient value is really pretty poor.

As I mentioned earlier, grains, pseudograins, and legumes are seeds. Seeds are an extraordinarily important part of plants – they’re needed for plants to reproduce. The nutrients in seeds aren’t meant for us, they’re meant to be used for growing a new plant.

Plants can’t protect their valuable seeds by running from predators or attacking them with sharp claws or teeth. Instead, their seeds have chemical defenses – compounds that protect their nutrients and cause harm to animals who eat them. These compounds are commonly referred to as antinutrients.

There are several types of antinutrients, including lectins, phytic acid (phytates), oxalic acid (oxalates), enzyme inhibitors, and saponins, each with unique harmful effects.

Lectins

Lectins are probably the most damaging and well-known antinutrients. You’ve probably heard of the most infamous lectin, gluten. Lectins inhibit nutrient absorption, cause bacterial overgrowth and systemic stress and inflammation, and damage our gut barrier, causing it to become permeable or “leaky” (2, 3, 4, 5, 6).

Gut permeability, or “leakiness,” allows undigested food particles and toxins to travel directly into the bloodstream, which can impair energy production and contribute to stress and inflammation (7, 8).

Phytic Acid and Oxalic Acid

Phytic acid and oxalic acid bind with calcium, magnesium, zinc, copper, potassium, iron, and other minerals, blocking their digestion and absorption in our guts and inhibiting our ability to use them (9, 10, 11). These minerals are vital for many processes, one of the most noteworthy being energy production.

Enzyme Inhibitors

Enzyme inhibitors block the enzymes in our guts that digest protein and starch, which prevents the digestion and absorption of protein and starches in the grains, pseudograins, and legumes, as well as in other foods we happen to be eating with them (9, 12, 13). Phytic acid also blocks some of these enzymes, further inhibiting the digestion of protein and starch (14, 15).

Saponins

Saponins, which are found mostly in pseudograins and legumes, inhibit protein-digesting enzymes, inhibit thyroid function (the regulator of our metabolism), and bind with and lower cholesterol (this isn’t beneficial, as we might be led to believe – I explain why here) (16, 17, 18).

 

Antinutrients No More

Somehow, the mainstream has found ways to spin the harmful effects of antinutrients into benefits. Impairing energy production and contributing to inflammation is considered “boosting immune function,” impairing starch digestion is considered “managing blood sugar,” and reducing cholesterol is, well, just reducing cholesterol, but this isn’t beneficial like we’ve been told.

If you ask me, it’s pretty clear that whole grains and legumes aren’t the health foods they’ve been made out to be. If anything, they appear to be worse than their obesity-, diabetes-, and heart disease-causing counterparts, refined grains. And this isn’t to mention the pesticides and GMOs that are ubiquitous among these crops.

But, it’s not all bad. In fact, grains and legumes can be prepared in ways that negate many of their negative effects. Cooking can deactivate a few of the antinutrients in these foods, but the traditional preparations of soaking, sprouting, and fermenting significantly reduce their antinutrient content, and may even alter their fiber composition (9, 19).

But if that doesn’t suit your fancy, you can skip these foods altogether!

Grains are most certainly not a necessary part of a healthy diet like they’ve been made out to be. Fruits and starch-containing foods that aren’t grains, including roots (carrots, yuca, turnips, etc.), tubers (potatoes and sweet potatoes), and vegetables in the gourd family (like squash and zucchini), are all great sources of carbohydrates with few antinutrients, if any.

(Note: some of these foods, like potatoes, do have antinutrients. But, they’re housed in the skins which can be easily removed.)

Also, while it is a grain, white rice is a relatively antinutrient-free carbohydrate source. This is because it’s stripped of its bran and hull, the parts of brown rice that contain most of the antinutrients.

Does all of this mean that if you eat any non-traditionally prepared grains, pseudograins, or legumes you can say goodbye to your health?

Of course not. But it does mean that their promotion as “health foods” is not supported, and we may want to reconsider how much of them we’re eating.

 

References

Grains and Legumes and Antinutrients, Oh My!

Despite the growing anti-grain movement, it’s still recommended that we consume 5-8 ounce equivalents or more of grains per day, and whole grains are still the face of the typical healthy diet (1).

Mainstream nutrition recommendations tell us that whole grains, pseudograins, and legumes are heart-healthy and promote a healthy weight. These food groups include foods like:

  • Wheat, corn, rye, barely, rice, millet, oats (grains)
  • Quinoa, amaranth, buckwheat (pseudograins)
  • Beans, soy, lentils, peanuts (legumes)

On the other hand, refined grains are the ones blamed for obesity, diabetes, and heart disease.

 

Holy Whole Grains vs. Evil Refined Grains

Let’s start with the basics.

Grains, pseudograins, and legumes are all seeds, which have 3 main components: bran, germ, and endosperm. The bran and germ contain most of the fiber and “nutrients,” and the endosperm is the carbohydrate-dense portion.

A whole grain is still intact – it contains all 3 of these components, while refined grains are stripped of the germ and bran, leaving only the endosperm.

So, the only difference between the “healthiest-of-all-foods” whole grains and the “inflammation-diabetes-obesity-and-heart-disease-causing” refined grains are the fiber and the “nutrients,” while the starch-containing endosperm is the same.

And, like whole grains, the “heart-healthy” pseudograins and legumes are full of fiber and “nutrients.”

But, it turns out that the fibers and “nutrients” found in these foods might not be so beneficial after all, leaving their supposed health-promoting effects in question.

 

Grains, Legumes, and Fiber

Whole grains, pseudograins, and legumes contain both soluble and insoluble fibers.

Soluble fibers are considered prebiotics because they feed our gut bacteria, whereas insoluble fibers are not digested by our gut bacteria and help to move food through our guts.

These fibers are considered beneficial because of ability to keep us full for longer, their prebiotic effects, and their colon cleansing effects.

But, these effects aren’t always so beneficial.

Keeping us full for longer might be favorable if we wanted to eat less, but eating less isn’t really beneficial unless we want to deprive ourselves of energy (Why “Eat Less and Exercise More” is the WORST Advice for Fat Loss and Health).

The ability for soluble fibers to feed our gut bacteria may sound healthy when it’s phrased as “feeding our good bacteria,” but this is more like wishful thinking. These fibers do feed our gut bacteria, but they feed the bad ones in addition to the good ones.

This isn’t a problem if our gut function and microbiome composition are optimal. But, if they aren’t optimal, which is extraordinarily common in modern times, this will exacerbate any gut dysfunction that’s going on.

(Fun fact: the gas that’s commonly associated with eating beans is a product of a suboptimal microbiome consuming soluble fiber)

On the other hand, the ability for insoluble fibers to move food through our gut is beneficial because gut motility is important for healthy gut function. But, this is a relatively trivial benefit in the context of grain consumption.

 

Grains, Legumes, and (Anti)nutrients

Whole grains, pseudograins, and legumes are touted for their nutrient content, specifically their vitamins, minerals, and protein. But when we consider their antinutrient content, their nutrient value is really pretty poor.

As I mentioned earlier, grains, pseudograins, and legumes are seeds. Seeds are an extraordinarily important part of plants – they’re needed for plants to reproduce. The nutrients in seeds aren’t meant for us, they’re meant to be used for growing a new plant.

Plants can’t protect their valuable seeds by running from predators or attacking them with sharp claws or teeth. Instead, their seeds have chemical defenses – compounds that protect their nutrients and cause harm to animals who eat them. These compounds are commonly referred to as antinutrients.

There are several types of antinutrients, including lectins, phytic acid (phytates), oxalic acid (oxalates), enzyme inhibitors, and saponins, each with unique harmful effects.

Lectins

Lectins are probably the most damaging and well-known antinutrients. You’ve probably heard of the most infamous lectin, gluten. Lectins inhibit nutrient absorption, cause bacterial overgrowth and systemic stress and inflammation, and damage our gut barrier, causing it to become permeable or “leaky” (2, 3, 4, 5, 6).

Gut permeability, or “leakiness,” allows undigested food particles and toxins to travel directly into the bloodstream, which can impair energy production and contribute to stress and inflammation (7, 8).

Phytic Acid and Oxalic Acid

Phytic acid and oxalic acid bind with calcium, magnesium, zinc, copper, potassium, iron, and other minerals, blocking their digestion and absorption in our guts and inhibiting our ability to use them (9, 10, 11). These minerals are vital for many processes, one of the most noteworthy being energy production.

Enzyme Inhibitors

Enzyme inhibitors block the enzymes in our guts that digest protein and starch, which prevents the digestion and absorption of protein and starches in the grains, pseudograins, and legumes, as well as in other foods we happen to be eating with them (9, 12, 13). Phytic acid also blocks some of these enzymes, further inhibiting the digestion of protein and starch (14, 15).

Saponins

Saponins, which are found mostly in pseudograins and legumes, inhibit protein-digesting enzymes, inhibit thyroid function (the regulator of our metabolism), and bind with and lower cholesterol (this isn’t beneficial, as we might be led to believe – I explain why here) (16, 17, 18).

 

Antinutrients No More

Somehow, the mainstream has found ways to spin the harmful effects of antinutrients into benefits. Impairing energy production and contributing to inflammation is considered “boosting immune function,” impairing starch digestion is considered “managing blood sugar,” and reducing cholesterol is, well, just reducing cholesterol, but this isn’t beneficial like we’ve been told.

If you ask me, it’s pretty clear that whole grains and legumes aren’t the health foods they’ve been made out to be. If anything, they appear to be worse than their obesity-, diabetes-, and heart disease-causing counterparts, refined grains. And this isn’t to mention the pesticides and GMOs that are ubiquitous among these crops.

But, it’s not all bad. In fact, grains and legumes can be prepared in ways that negate many of their negative effects. Cooking can deactivate a few of the antinutrients in these foods, but the traditional preparations of soaking, sprouting, and fermenting significantly reduce their antinutrient content, and may even alter their fiber composition (9, 19).

But if that doesn’t suit your fancy, you can skip these foods altogether!

Grains are most certainly not a necessary part of a healthy diet like they’ve been made out to be. Fruits and starch-containing foods that aren’t grains, including roots (carrots, yuca, turnips, etc.), tubers (potatoes and sweet potatoes), and vegetables in the gourd family (like squash and zucchini), are all great sources of carbohydrates with few antinutrients, if any.

(Note: some of these foods, like potatoes, do have antinutrients. But, they’re housed in the skins which can be easily removed.)

Also, while it is a grain, white rice is a relatively antinutrient-free carbohydrate source. This is because it’s stripped of its bran and hull, the parts of brown rice that contain most of the antinutrients.

Does all of this mean that if you eat any non-traditionally prepared grains, pseudograins, or legumes you can say goodbye to your health?

Of course not. But it does mean that their promotion as “health foods” is not supported, and we may want to reconsider how much of them we’re eating.

 

References

Grains and Legumes and Antinutrients, Oh My!

Despite the growing anti-grain movement, it’s still recommended that we consume 5-8 ounce equivalents or more of grains per day, and whole grains are still the face of the typical healthy diet (1).

Mainstream nutrition recommendations tell us that whole grains, pseudograins, and legumes are heart-healthy and promote a healthy weight. These food groups include foods like:

  • Wheat, corn, rye, barely, rice, millet, oats (grains)
  • Quinoa, amaranth, buckwheat (pseudograins)
  • Beans, soy, lentils, peanuts (legumes)

On the other hand, refined grains are the ones blamed for obesity, diabetes, and heart disease.

 

Holy Whole Grains vs. Evil Refined Grains

Let’s start with the basics.

Grains, pseudograins, and legumes are all seeds, which have 3 main components: bran, germ, and endosperm. The bran and germ contain most of the fiber and “nutrients,” and the endosperm is the carbohydrate-dense portion.

A whole grain is still intact – it contains all 3 of these components, while refined grains are stripped of the germ and bran, leaving only the endosperm.

So, the only difference between the “healthiest-of-all-foods” whole grains and the “inflammation-diabetes-obesity-and-heart-disease-causing” refined grains are the fiber and the “nutrients,” while the starch-containing endosperm is the same.

And, like whole grains, the “heart-healthy” pseudograins and legumes are full of fiber and “nutrients.”

But, it turns out that the fibers and “nutrients” found in these foods might not be so beneficial after all, leaving their supposed health-promoting effects in question.

 

Grains, Legumes, and Fiber

Whole grains, pseudograins, and legumes contain both soluble and insoluble fibers.

Soluble fibers are considered prebiotics because they feed our gut bacteria, whereas insoluble fibers are not digested by our gut bacteria and help to move food through our guts.

These fibers are considered beneficial because of ability to keep us full for longer, their prebiotic effects, and their colon cleansing effects.

But, these effects aren’t always so beneficial.

Keeping us full for longer might be favorable if we wanted to eat less, but eating less isn’t really beneficial unless we want to deprive ourselves of energy (Why “Eat Less and Exercise More” is the WORST Advice for Fat Loss and Health).

The ability for soluble fibers to feed our gut bacteria may sound healthy when it’s phrased as “feeding our good bacteria,” but this is more like wishful thinking. These fibers do feed our gut bacteria, but they feed the bad ones in addition to the good ones.

This isn’t a problem if our gut function and microbiome composition are optimal. But, if they aren’t optimal, which is extraordinarily common in modern times, this will exacerbate any gut dysfunction that’s going on.

(Fun fact: the gas that’s commonly associated with eating beans is a product of a suboptimal microbiome consuming soluble fiber)

On the other hand, the ability for insoluble fibers to move food through our gut is beneficial because gut motility is important for healthy gut function. But, this is a relatively trivial benefit in the context of grain consumption.

 

Grains, Legumes, and (Anti)nutrients

Whole grains, pseudograins, and legumes are touted for their nutrient content, specifically their vitamins, minerals, and protein. But when we consider their antinutrient content, their nutrient value is really pretty poor.

As I mentioned earlier, grains, pseudograins, and legumes are seeds. Seeds are an extraordinarily important part of plants – they’re needed for plants to reproduce. The nutrients in seeds aren’t meant for us, they’re meant to be used for growing a new plant.

Plants can’t protect their valuable seeds by running from predators or attacking them with sharp claws or teeth. Instead, their seeds have chemical defenses – compounds that protect their nutrients and cause harm to animals who eat them. These compounds are commonly referred to as antinutrients.

There are several types of antinutrients, including lectins, phytic acid (phytates), oxalic acid (oxalates), enzyme inhibitors, and saponins, each with unique harmful effects.

Lectins

Lectins are probably the most damaging and well-known antinutrients. You’ve probably heard of the most infamous lectin, gluten. Lectins inhibit nutrient absorption, cause bacterial overgrowth and systemic stress and inflammation, and damage our gut barrier, causing it to become permeable or “leaky” (2, 3, 4, 5, 6).

Gut permeability, or “leakiness,” allows undigested food particles and toxins to travel directly into the bloodstream, which can impair energy production and contribute to stress and inflammation (7, 8).

Phytic Acid and Oxalic Acid

Phytic acid and oxalic acid bind with calcium, magnesium, zinc, copper, potassium, iron, and other minerals, blocking their digestion and absorption in our guts and inhibiting our ability to use them (9, 10, 11). These minerals are vital for many processes, one of the most noteworthy being energy production.

Enzyme Inhibitors

Enzyme inhibitors block the enzymes in our guts that digest protein and starch, which prevents the digestion and absorption of protein and starches in the grains, pseudograins, and legumes, as well as in other foods we happen to be eating with them (9, 12, 13). Phytic acid also blocks some of these enzymes, further inhibiting the digestion of protein and starch (14, 15).

Saponins

Saponins, which are found mostly in pseudograins and legumes, inhibit protein-digesting enzymes, inhibit thyroid function (the regulator of our metabolism), and bind with and lower cholesterol (this isn’t beneficial, as we might be led to believe – I explain why here) (16, 17, 18).

 

Antinutrients No More

Somehow, the mainstream has found ways to spin the harmful effects of antinutrients into benefits. Impairing energy production and contributing to inflammation is considered “boosting immune function,” impairing starch digestion is considered “managing blood sugar,” and reducing cholesterol is, well, just reducing cholesterol, but this isn’t beneficial like we’ve been told.

If you ask me, it’s pretty clear that whole grains and legumes aren’t the health foods they’ve been made out to be. If anything, they appear to be worse than their obesity-, diabetes-, and heart disease-causing counterparts, refined grains. And this isn’t to mention the pesticides and GMOs that are ubiquitous among these crops.

But, it’s not all bad. In fact, grains and legumes can be prepared in ways that negate many of their negative effects. Cooking can deactivate a few of the antinutrients in these foods, but the traditional preparations of soaking, sprouting, and fermenting significantly reduce their antinutrient content, and may even alter their fiber composition (9, 19).

But if that doesn’t suit your fancy, you can skip these foods altogether!

Grains are most certainly not a necessary part of a healthy diet like they’ve been made out to be. Fruits and starch-containing foods that aren’t grains, including roots (carrots, yuca, turnips, etc.), tubers (potatoes and sweet potatoes), and vegetables in the gourd family (like squash and zucchini), are all great sources of carbohydrates with few antinutrients, if any.

(Note: some of these foods, like potatoes, do have antinutrients. But, they’re housed in the skins which can be easily removed.)

Also, while it is a grain, white rice is a relatively antinutrient-free carbohydrate source. This is because it’s stripped of its bran and hull, the parts of brown rice that contain most of the antinutrients.

Does all of this mean that if you eat any non-traditionally prepared grains, pseudograins, or legumes you can say goodbye to your health?

Of course not. But it does mean that their promotion as “health foods” is not supported, and we may want to reconsider how much of them we’re eating.

 

References

Grains and Legumes and Antinutrients, Oh My!

Despite the growing anti-grain movement, it’s still recommended that we consume 5-8 ounce equivalents or more of grains per day, and whole grains are still the face of the typical healthy diet (1).

Mainstream nutrition recommendations tell us that whole grains, pseudograins, and legumes are heart-healthy and promote a healthy weight. These food groups include foods like:

  • Wheat, corn, rye, barely, rice, millet, oats (grains)
  • Quinoa, amaranth, buckwheat (pseudograins)
  • Beans, soy, lentils, peanuts (legumes)

On the other hand, refined grains are the ones blamed for obesity, diabetes, and heart disease.

 

Holy Whole Grains vs. Evil Refined Grains

Let’s start with the basics.

Grains, pseudograins, and legumes are all seeds, which have 3 main components: bran, germ, and endosperm. The bran and germ contain most of the fiber and “nutrients,” and the endosperm is the carbohydrate-dense portion.

A whole grain is still intact – it contains all 3 of these components, while refined grains are stripped of the germ and bran, leaving only the endosperm.

So, the only difference between the “healthiest-of-all-foods” whole grains and the “inflammation-diabetes-obesity-and-heart-disease-causing” refined grains are the fiber and the “nutrients,” while the starch-containing endosperm is the same.

And, like whole grains, the “heart-healthy” pseudograins and legumes are full of fiber and “nutrients.”

But, it turns out that the fibers and “nutrients” found in these foods might not be so beneficial after all, leaving their supposed health-promoting effects in question.

 

Grains, Legumes, and Fiber

Whole grains, pseudograins, and legumes contain both soluble and insoluble fibers.

Soluble fibers are considered prebiotics because they feed our gut bacteria, whereas insoluble fibers are not digested by our gut bacteria and help to move food through our guts.

These fibers are considered beneficial because of ability to keep us full for longer, their prebiotic effects, and their colon cleansing effects.

But, these effects aren’t always so beneficial.

Keeping us full for longer might be favorable if we wanted to eat less, but eating less isn’t really beneficial unless we want to deprive ourselves of energy (Why “Eat Less and Exercise More” is the WORST Advice for Fat Loss and Health).

The ability for soluble fibers to feed our gut bacteria may sound healthy when it’s phrased as “feeding our good bacteria,” but this is more like wishful thinking. These fibers do feed our gut bacteria, but they feed the bad ones in addition to the good ones.

This isn’t a problem if our gut function and microbiome composition are optimal. But, if they aren’t optimal, which is extraordinarily common in modern times, this will exacerbate any gut dysfunction that’s going on.

(Fun fact: the gas that’s commonly associated with eating beans is a product of a suboptimal microbiome consuming soluble fiber)

On the other hand, the ability for insoluble fibers to move food through our gut is beneficial because gut motility is important for healthy gut function. But, this is a relatively trivial benefit in the context of grain consumption.

 

Grains, Legumes, and (Anti)nutrients

Whole grains, pseudograins, and legumes are touted for their nutrient content, specifically their vitamins, minerals, and protein. But when we consider their antinutrient content, their nutrient value is really pretty poor.

As I mentioned earlier, grains, pseudograins, and legumes are seeds. Seeds are an extraordinarily important part of plants – they’re needed for plants to reproduce. The nutrients in seeds aren’t meant for us, they’re meant to be used for growing a new plant.

Plants can’t protect their valuable seeds by running from predators or attacking them with sharp claws or teeth. Instead, their seeds have chemical defenses – compounds that protect their nutrients and cause harm to animals who eat them. These compounds are commonly referred to as antinutrients.

There are several types of antinutrients, including lectins, phytic acid (phytates), oxalic acid (oxalates), enzyme inhibitors, and saponins, each with unique harmful effects.

Lectins

Lectins are probably the most damaging and well-known antinutrients. You’ve probably heard of the most infamous lectin, gluten. Lectins inhibit nutrient absorption, cause bacterial overgrowth and systemic stress and inflammation, and damage our gut barrier, causing it to become permeable or “leaky” (2, 3, 4, 5, 6).

Gut permeability, or “leakiness,” allows undigested food particles and toxins to travel directly into the bloodstream, which can impair energy production and contribute to stress and inflammation (7, 8).

Phytic Acid and Oxalic Acid

Phytic acid and oxalic acid bind with calcium, magnesium, zinc, copper, potassium, iron, and other minerals, blocking their digestion and absorption in our guts and inhibiting our ability to use them (9, 10, 11). These minerals are vital for many processes, one of the most noteworthy being energy production.

Enzyme Inhibitors

Enzyme inhibitors block the enzymes in our guts that digest protein and starch, which prevents the digestion and absorption of protein and starches in the grains, pseudograins, and legumes, as well as in other foods we happen to be eating with them (9, 12, 13). Phytic acid also blocks some of these enzymes, further inhibiting the digestion of protein and starch (14, 15).

Saponins

Saponins, which are found mostly in pseudograins and legumes, inhibit protein-digesting enzymes, inhibit thyroid function (the regulator of our metabolism), and bind with and lower cholesterol (this isn’t beneficial, as we might be led to believe – I explain why here) (16, 17, 18).

 

Antinutrients No More

Somehow, the mainstream has found ways to spin the harmful effects of antinutrients into benefits. Impairing energy production and contributing to inflammation is considered “boosting immune function,” impairing starch digestion is considered “managing blood sugar,” and reducing cholesterol is, well, just reducing cholesterol, but this isn’t beneficial like we’ve been told.

If you ask me, it’s pretty clear that whole grains and legumes aren’t the health foods they’ve been made out to be. If anything, they appear to be worse than their obesity-, diabetes-, and heart disease-causing counterparts, refined grains. And this isn’t to mention the pesticides and GMOs that are ubiquitous among these crops.

But, it’s not all bad. In fact, grains and legumes can be prepared in ways that negate many of their negative effects. Cooking can deactivate a few of the antinutrients in these foods, but the traditional preparations of soaking, sprouting, and fermenting significantly reduce their antinutrient content, and may even alter their fiber composition (9, 19).

But if that doesn’t suit your fancy, you can skip these foods altogether!

Grains are most certainly not a necessary part of a healthy diet like they’ve been made out to be. Fruits and starch-containing foods that aren’t grains, including roots (carrots, yuca, turnips, etc.), tubers (potatoes and sweet potatoes), and vegetables in the gourd family (like squash and zucchini), are all great sources of carbohydrates with few antinutrients, if any.

(Note: some of these foods, like potatoes, do have antinutrients. But, they’re housed in the skins which can be easily removed.)

Also, while it is a grain, white rice is a relatively antinutrient-free carbohydrate source. This is because it’s stripped of its bran and hull, the parts of brown rice that contain most of the antinutrients.

Does all of this mean that if you eat any non-traditionally prepared grains, pseudograins, or legumes you can say goodbye to your health?

Of course not. But it does mean that their promotion as “health foods” is not supported, and we may want to reconsider how much of them we’re eating.

 

References

Grains and Legumes and Antinutrients, Oh My!

Despite the growing anti-grain movement, it’s still recommended that we consume 5-8 ounce equivalents or more of grains per day, and whole grains are still the face of the typical healthy diet (1).

Mainstream nutrition recommendations tell us that whole grains, pseudograins, and legumes are heart-healthy and promote a healthy weight. These food groups include foods like:

  • Wheat, corn, rye, barely, rice, millet, oats (grains)
  • Quinoa, amaranth, buckwheat (pseudograins)
  • Beans, soy, lentils, peanuts (legumes)

On the other hand, refined grains are the ones blamed for obesity, diabetes, and heart disease.

 

Holy Whole Grains vs. Evil Refined Grains

Let’s start with the basics.

Grains, pseudograins, and legumes are all seeds, which have 3 main components: bran, germ, and endosperm. The bran and germ contain most of the fiber and “nutrients,” and the endosperm is the carbohydrate-dense portion.

A whole grain is still intact – it contains all 3 of these components, while refined grains are stripped of the germ and bran, leaving only the endosperm.

So, the only difference between the “healthiest-of-all-foods” whole grains and the “inflammation-diabetes-obesity-and-heart-disease-causing” refined grains are the fiber and the “nutrients,” while the starch-containing endosperm is the same.

And, like whole grains, the “heart-healthy” pseudograins and legumes are full of fiber and “nutrients.”

But, it turns out that the fibers and “nutrients” found in these foods might not be so beneficial after all, leaving their supposed health-promoting effects in question.

 

Grains, Legumes, and Fiber

Whole grains, pseudograins, and legumes contain both soluble and insoluble fibers.

Soluble fibers are considered prebiotics because they feed our gut bacteria, whereas insoluble fibers are not digested by our gut bacteria and help to move food through our guts.

These fibers are considered beneficial because of ability to keep us full for longer, their prebiotic effects, and their colon cleansing effects.

But, these effects aren’t always so beneficial.

Keeping us full for longer might be favorable if we wanted to eat less, but eating less isn’t really beneficial unless we want to deprive ourselves of energy (Why “Eat Less and Exercise More” is the WORST Advice for Fat Loss and Health).

The ability for soluble fibers to feed our gut bacteria may sound healthy when it’s phrased as “feeding our good bacteria,” but this is more like wishful thinking. These fibers do feed our gut bacteria, but they feed the bad ones in addition to the good ones.

This isn’t a problem if our gut function and microbiome composition are optimal. But, if they aren’t optimal, which is extraordinarily common in modern times, this will exacerbate any gut dysfunction that’s going on.

(Fun fact: the gas that’s commonly associated with eating beans is a product of a suboptimal microbiome consuming soluble fiber)

On the other hand, the ability for insoluble fibers to move food through our gut is beneficial because gut motility is important for healthy gut function. But, this is a relatively trivial benefit in the context of grain consumption.

 

Grains, Legumes, and (Anti)nutrients

Whole grains, pseudograins, and legumes are touted for their nutrient content, specifically their vitamins, minerals, and protein. But when we consider their antinutrient content, their nutrient value is really pretty poor.

As I mentioned earlier, grains, pseudograins, and legumes are seeds. Seeds are an extraordinarily important part of plants – they’re needed for plants to reproduce. The nutrients in seeds aren’t meant for us, they’re meant to be used for growing a new plant.

Plants can’t protect their valuable seeds by running from predators or attacking them with sharp claws or teeth. Instead, their seeds have chemical defenses – compounds that protect their nutrients and cause harm to animals who eat them. These compounds are commonly referred to as antinutrients.

There are several types of antinutrients, including lectins, phytic acid (phytates), oxalic acid (oxalates), enzyme inhibitors, and saponins, each with unique harmful effects.

Lectins

Lectins are probably the most damaging and well-known antinutrients. You’ve probably heard of the most infamous lectin, gluten. Lectins inhibit nutrient absorption, cause bacterial overgrowth and systemic stress and inflammation, and damage our gut barrier, causing it to become permeable or “leaky” (2, 3, 4, 5, 6).

Gut permeability, or “leakiness,” allows undigested food particles and toxins to travel directly into the bloodstream, which can impair energy production and contribute to stress and inflammation (7, 8).

Phytic Acid and Oxalic Acid

Phytic acid and oxalic acid bind with calcium, magnesium, zinc, copper, potassium, iron, and other minerals, blocking their digestion and absorption in our guts and inhibiting our ability to use them (9, 10, 11). These minerals are vital for many processes, one of the most noteworthy being energy production.

Enzyme Inhibitors

Enzyme inhibitors block the enzymes in our guts that digest protein and starch, which prevents the digestion and absorption of protein and starches in the grains, pseudograins, and legumes, as well as in other foods we happen to be eating with them (9, 12, 13). Phytic acid also blocks some of these enzymes, further inhibiting the digestion of protein and starch (14, 15).

Saponins

Saponins, which are found mostly in pseudograins and legumes, inhibit protein-digesting enzymes, inhibit thyroid function (the regulator of our metabolism), and bind with and lower cholesterol (this isn’t beneficial, as we might be led to believe – I explain why here) (16, 17, 18).

 

Antinutrients No More

Somehow, the mainstream has found ways to spin the harmful effects of antinutrients into benefits. Impairing energy production and contributing to inflammation is considered “boosting immune function,” impairing starch digestion is considered “managing blood sugar,” and reducing cholesterol is, well, just reducing cholesterol, but this isn’t beneficial like we’ve been told.

If you ask me, it’s pretty clear that whole grains and legumes aren’t the health foods they’ve been made out to be. If anything, they appear to be worse than their obesity-, diabetes-, and heart disease-causing counterparts, refined grains. And this isn’t to mention the pesticides and GMOs that are ubiquitous among these crops.

But, it’s not all bad. In fact, grains and legumes can be prepared in ways that negate many of their negative effects. Cooking can deactivate a few of the antinutrients in these foods, but the traditional preparations of soaking, sprouting, and fermenting significantly reduce their antinutrient content, and may even alter their fiber composition (9, 19).

But if that doesn’t suit your fancy, you can skip these foods altogether!

Grains are most certainly not a necessary part of a healthy diet like they’ve been made out to be. Fruits and starch-containing foods that aren’t grains, including roots (carrots, yuca, turnips, etc.), tubers (potatoes and sweet potatoes), and vegetables in the gourd family (like squash and zucchini), are all great sources of carbohydrates with few antinutrients, if any.

(Note: some of these foods, like potatoes, do have antinutrients. But, they’re housed in the skins which can be easily removed.)

Also, while it is a grain, white rice is a relatively antinutrient-free carbohydrate source. This is because it’s stripped of its bran and hull, the parts of brown rice that contain most of the antinutrients.

Does all of this mean that if you eat any non-traditionally prepared grains, pseudograins, or legumes you can say goodbye to your health?

Of course not. But it does mean that their promotion as “health foods” is not supported, and we may want to reconsider how much of them we’re eating.

 

References

Grains and Legumes and Antinutrients, Oh My!

Despite the growing anti-grain movement, it’s still recommended that we consume 5-8 ounce equivalents or more of grains per day, and whole grains are still the face of the typical healthy diet (1).

Mainstream nutrition recommendations tell us that whole grains, pseudograins, and legumes are heart-healthy and promote a healthy weight. These food groups include foods like:

  • Wheat, corn, rye, barely, rice, millet, oats (grains)
  • Quinoa, amaranth, buckwheat (pseudograins)
  • Beans, soy, lentils, peanuts (legumes)

On the other hand, refined grains are the ones blamed for obesity, diabetes, and heart disease.

 

Holy Whole Grains vs. Evil Refined Grains

Let’s start with the basics.

Grains, pseudograins, and legumes are all seeds, which have 3 main components: bran, germ, and endosperm. The bran and germ contain most of the fiber and “nutrients,” and the endosperm is the carbohydrate-dense portion.

A whole grain is still intact – it contains all 3 of these components, while refined grains are stripped of the germ and bran, leaving only the endosperm.

So, the only difference between the “healthiest-of-all-foods” whole grains and the “inflammation-diabetes-obesity-and-heart-disease-causing” refined grains are the fiber and the “nutrients,” while the starch-containing endosperm is the same.

And, like whole grains, the “heart-healthy” pseudograins and legumes are full of fiber and “nutrients.”

But, it turns out that the fibers and “nutrients” found in these foods might not be so beneficial after all, leaving their supposed health-promoting effects in question.

 

Grains, Legumes, and Fiber

Whole grains, pseudograins, and legumes contain both soluble and insoluble fibers.

Soluble fibers are considered prebiotics because they feed our gut bacteria, whereas insoluble fibers are not digested by our gut bacteria and help to move food through our guts.

These fibers are considered beneficial because of ability to keep us full for longer, their prebiotic effects, and their colon cleansing effects.

But, these effects aren’t always so beneficial.

Keeping us full for longer might be favorable if we wanted to eat less, but eating less isn’t really beneficial unless we want to deprive ourselves of energy (Why “Eat Less and Exercise More” is the WORST Advice for Fat Loss and Health).

The ability for soluble fibers to feed our gut bacteria may sound healthy when it’s phrased as “feeding our good bacteria,” but this is more like wishful thinking. These fibers do feed our gut bacteria, but they feed the bad ones in addition to the good ones.

This isn’t a problem if our gut function and microbiome composition are optimal. But, if they aren’t optimal, which is extraordinarily common in modern times, this will exacerbate any gut dysfunction that’s going on.

(Fun fact: the gas that’s commonly associated with eating beans is a product of a suboptimal microbiome consuming soluble fiber)

On the other hand, the ability for insoluble fibers to move food through our gut is beneficial because gut motility is important for healthy gut function. But, this is a relatively trivial benefit in the context of grain consumption.

 

Grains, Legumes, and (Anti)nutrients

Whole grains, pseudograins, and legumes are touted for their nutrient content, specifically their vitamins, minerals, and protein. But when we consider their antinutrient content, their nutrient value is really pretty poor.

As I mentioned earlier, grains, pseudograins, and legumes are seeds. Seeds are an extraordinarily important part of plants – they’re needed for plants to reproduce. The nutrients in seeds aren’t meant for us, they’re meant to be used for growing a new plant.

Plants can’t protect their valuable seeds by running from predators or attacking them with sharp claws or teeth. Instead, their seeds have chemical defenses – compounds that protect their nutrients and cause harm to animals who eat them. These compounds are commonly referred to as antinutrients.

There are several types of antinutrients, including lectins, phytic acid (phytates), oxalic acid (oxalates), enzyme inhibitors, and saponins, each with unique harmful effects.

Lectins

Lectins are probably the most damaging and well-known antinutrients. You’ve probably heard of the most infamous lectin, gluten. Lectins inhibit nutrient absorption, cause bacterial overgrowth and systemic stress and inflammation, and damage our gut barrier, causing it to become permeable or “leaky” (2, 3, 4, 5, 6).

Gut permeability, or “leakiness,” allows undigested food particles and toxins to travel directly into the bloodstream, which can impair energy production and contribute to stress and inflammation (7, 8).

Phytic Acid and Oxalic Acid

Phytic acid and oxalic acid bind with calcium, magnesium, zinc, copper, potassium, iron, and other minerals, blocking their digestion and absorption in our guts and inhibiting our ability to use them (9, 10, 11). These minerals are vital for many processes, one of the most noteworthy being energy production.

Enzyme Inhibitors

Enzyme inhibitors block the enzymes in our guts that digest protein and starch, which prevents the digestion and absorption of protein and starches in the grains, pseudograins, and legumes, as well as in other foods we happen to be eating with them (9, 12, 13). Phytic acid also blocks some of these enzymes, further inhibiting the digestion of protein and starch (14, 15).

Saponins

Saponins, which are found mostly in pseudograins and legumes, inhibit protein-digesting enzymes, inhibit thyroid function (the regulator of our metabolism), and bind with and lower cholesterol (this isn’t beneficial, as we might be led to believe – I explain why here) (16, 17, 18).

 

Antinutrients No More

Somehow, the mainstream has found ways to spin the harmful effects of antinutrients into benefits. Impairing energy production and contributing to inflammation is considered “boosting immune function,” impairing starch digestion is considered “managing blood sugar,” and reducing cholesterol is, well, just reducing cholesterol, but this isn’t beneficial like we’ve been told.

If you ask me, it’s pretty clear that whole grains and legumes aren’t the health foods they’ve been made out to be. If anything, they appear to be worse than their obesity-, diabetes-, and heart disease-causing counterparts, refined grains. And this isn’t to mention the pesticides and GMOs that are ubiquitous among these crops.

But, it’s not all bad. In fact, grains and legumes can be prepared in ways that negate many of their negative effects. Cooking can deactivate a few of the antinutrients in these foods, but the traditional preparations of soaking, sprouting, and fermenting significantly reduce their antinutrient content, and may even alter their fiber composition (9, 19).

But if that doesn’t suit your fancy, you can skip these foods altogether!

Grains are most certainly not a necessary part of a healthy diet like they’ve been made out to be. Fruits and starch-containing foods that aren’t grains, including roots (carrots, yuca, turnips, etc.), tubers (potatoes and sweet potatoes), and vegetables in the gourd family (like squash and zucchini), are all great sources of carbohydrates with few antinutrients, if any.

(Note: some of these foods, like potatoes, do have antinutrients. But, they’re housed in the skins which can be easily removed.)

Also, while it is a grain, white rice is a relatively antinutrient-free carbohydrate source. This is because it’s stripped of its bran and hull, the parts of brown rice that contain most of the antinutrients.

Does all of this mean that if you eat any non-traditionally prepared grains, pseudograins, or legumes you can say goodbye to your health?

Of course not. But it does mean that their promotion as “health foods” is not supported, and we may want to reconsider how much of them we’re eating.

 

References

Grains and Legumes and Antinutrients, Oh My!

Despite the growing anti-grain movement, it’s still recommended that we consume 5-8 ounce equivalents or more of grains per day, and whole grains are still the face of the typical healthy diet (1).

Mainstream nutrition recommendations tell us that whole grains, pseudograins, and legumes are heart-healthy and promote a healthy weight. These food groups include foods like:

  • Wheat, corn, rye, barely, rice, millet, oats (grains)
  • Quinoa, amaranth, buckwheat (pseudograins)
  • Beans, soy, lentils, peanuts (legumes)

On the other hand, refined grains are the ones blamed for obesity, diabetes, and heart disease.

 

Holy Whole Grains vs. Evil Refined Grains

Let’s start with the basics.

Grains, pseudograins, and legumes are all seeds, which have 3 main components: bran, germ, and endosperm. The bran and germ contain most of the fiber and “nutrients,” and the endosperm is the carbohydrate-dense portion.

A whole grain is still intact – it contains all 3 of these components, while refined grains are stripped of the germ and bran, leaving only the endosperm.

So, the only difference between the “healthiest-of-all-foods” whole grains and the “inflammation-diabetes-obesity-and-heart-disease-causing” refined grains are the fiber and the “nutrients,” while the starch-containing endosperm is the same.

And, like whole grains, the “heart-healthy” pseudograins and legumes are full of fiber and “nutrients.”

But, it turns out that the fibers and “nutrients” found in these foods might not be so beneficial after all, leaving their supposed health-promoting effects in question.

 

Grains, Legumes, and Fiber

Whole grains, pseudograins, and legumes contain both soluble and insoluble fibers.

Soluble fibers are considered prebiotics because they feed our gut bacteria, whereas insoluble fibers are not digested by our gut bacteria and help to move food through our guts.

These fibers are considered beneficial because of ability to keep us full for longer, their prebiotic effects, and their colon cleansing effects.

But, these effects aren’t always so beneficial.

Keeping us full for longer might be favorable if we wanted to eat less, but eating less isn’t really beneficial unless we want to deprive ourselves of energy (Why “Eat Less and Exercise More” is the WORST Advice for Fat Loss and Health).

The ability for soluble fibers to feed our gut bacteria may sound healthy when it’s phrased as “feeding our good bacteria,” but this is more like wishful thinking. These fibers do feed our gut bacteria, but they feed the bad ones in addition to the good ones.

This isn’t a problem if our gut function and microbiome composition are optimal. But, if they aren’t optimal, which is extraordinarily common in modern times, this will exacerbate any gut dysfunction that’s going on.

(Fun fact: the gas that’s commonly associated with eating beans is a product of a suboptimal microbiome consuming soluble fiber)

On the other hand, the ability for insoluble fibers to move food through our gut is beneficial because gut motility is important for healthy gut function. But, this is a relatively trivial benefit in the context of grain consumption.

 

Grains, Legumes, and (Anti)nutrients

Whole grains, pseudograins, and legumes are touted for their nutrient content, specifically their vitamins, minerals, and protein. But when we consider their antinutrient content, their nutrient value is really pretty poor.

As I mentioned earlier, grains, pseudograins, and legumes are seeds. Seeds are an extraordinarily important part of plants – they’re needed for plants to reproduce. The nutrients in seeds aren’t meant for us, they’re meant to be used for growing a new plant.

Plants can’t protect their valuable seeds by running from predators or attacking them with sharp claws or teeth. Instead, their seeds have chemical defenses – compounds that protect their nutrients and cause harm to animals who eat them. These compounds are commonly referred to as antinutrients.

There are several types of antinutrients, including lectins, phytic acid (phytates), oxalic acid (oxalates), enzyme inhibitors, and saponins, each with unique harmful effects.

Lectins

Lectins are probably the most damaging and well-known antinutrients. You’ve probably heard of the most infamous lectin, gluten. Lectins inhibit nutrient absorption, cause bacterial overgrowth and systemic stress and inflammation, and damage our gut barrier, causing it to become permeable or “leaky” (2, 3, 4, 5, 6).

Gut permeability, or “leakiness,” allows undigested food particles and toxins to travel directly into the bloodstream, which can impair energy production and contribute to stress and inflammation (7, 8).

Phytic Acid and Oxalic Acid

Phytic acid and oxalic acid bind with calcium, magnesium, zinc, copper, potassium, iron, and other minerals, blocking their digestion and absorption in our guts and inhibiting our ability to use them (9, 10, 11). These minerals are vital for many processes, one of the most noteworthy being energy production.

Enzyme Inhibitors

Enzyme inhibitors block the enzymes in our guts that digest protein and starch, which prevents the digestion and absorption of protein and starches in the grains, pseudograins, and legumes, as well as in other foods we happen to be eating with them (9, 12, 13). Phytic acid also blocks some of these enzymes, further inhibiting the digestion of protein and starch (14, 15).

Saponins

Saponins, which are found mostly in pseudograins and legumes, inhibit protein-digesting enzymes, inhibit thyroid function (the regulator of our metabolism), and bind with and lower cholesterol (this isn’t beneficial, as we might be led to believe – I explain why here) (16, 17, 18).

 

Antinutrients No More

Somehow, the mainstream has found ways to spin the harmful effects of antinutrients into benefits. Impairing energy production and contributing to inflammation is considered “boosting immune function,” impairing starch digestion is considered “managing blood sugar,” and reducing cholesterol is, well, just reducing cholesterol, but this isn’t beneficial like we’ve been told.

If you ask me, it’s pretty clear that whole grains and legumes aren’t the health foods they’ve been made out to be. If anything, they appear to be worse than their obesity-, diabetes-, and heart disease-causing counterparts, refined grains. And this isn’t to mention the pesticides and GMOs that are ubiquitous among these crops.

But, it’s not all bad. In fact, grains and legumes can be prepared in ways that negate many of their negative effects. Cooking can deactivate a few of the antinutrients in these foods, but the traditional preparations of soaking, sprouting, and fermenting significantly reduce their antinutrient content, and may even alter their fiber composition (9, 19).

But if that doesn’t suit your fancy, you can skip these foods altogether!

Grains are most certainly not a necessary part of a healthy diet like they’ve been made out to be. Fruits and starch-containing foods that aren’t grains, including roots (carrots, yuca, turnips, etc.), tubers (potatoes and sweet potatoes), and vegetables in the gourd family (like squash and zucchini), are all great sources of carbohydrates with few antinutrients, if any.

(Note: some of these foods, like potatoes, do have antinutrients. But, they’re housed in the skins which can be easily removed.)

Also, while it is a grain, white rice is a relatively antinutrient-free carbohydrate source. This is because it’s stripped of its bran and hull, the parts of brown rice that contain most of the antinutrients.

Does all of this mean that if you eat any non-traditionally prepared grains, pseudograins, or legumes you can say goodbye to your health?

Of course not. But it does mean that their promotion as “health foods” is not supported, and we may want to reconsider how much of them we’re eating.

 

References

Grains and Legumes and Antinutrients, Oh My!

Despite the growing anti-grain movement, it’s still recommended that we consume 5-8 ounce equivalents or more of grains per day, and whole grains are still the face of the typical healthy diet (1).

Mainstream nutrition recommendations tell us that whole grains, pseudograins, and legumes are heart-healthy and promote a healthy weight. These food groups include foods like:

  • Wheat, corn, rye, barely, rice, millet, oats (grains)
  • Quinoa, amaranth, buckwheat (pseudograins)
  • Beans, soy, lentils, peanuts (legumes)

On the other hand, refined grains are the ones blamed for obesity, diabetes, and heart disease.

 

Holy Whole Grains vs. Evil Refined Grains

Let’s start with the basics.

Grains, pseudograins, and legumes are all seeds, which have 3 main components: bran, germ, and endosperm. The bran and germ contain most of the fiber and “nutrients,” and the endosperm is the carbohydrate-dense portion.

A whole grain is still intact – it contains all 3 of these components, while refined grains are stripped of the germ and bran, leaving only the endosperm.

So, the only difference between the “healthiest-of-all-foods” whole grains and the “inflammation-diabetes-obesity-and-heart-disease-causing” refined grains are the fiber and the “nutrients,” while the starch-containing endosperm is the same.

And, like whole grains, the “heart-healthy” pseudograins and legumes are full of fiber and “nutrients.”

But, it turns out that the fibers and “nutrients” found in these foods might not be so beneficial after all, leaving their supposed health-promoting effects in question.

 

Grains, Legumes, and Fiber

Whole grains, pseudograins, and legumes contain both soluble and insoluble fibers.

Soluble fibers are considered prebiotics because they feed our gut bacteria, whereas insoluble fibers are not digested by our gut bacteria and help to move food through our guts.

These fibers are considered beneficial because of ability to keep us full for longer, their prebiotic effects, and their colon cleansing effects.

But, these effects aren’t always so beneficial.

Keeping us full for longer might be favorable if we wanted to eat less, but eating less isn’t really beneficial unless we want to deprive ourselves of energy (Why “Eat Less and Exercise More” is the WORST Advice for Fat Loss and Health).

The ability for soluble fibers to feed our gut bacteria may sound healthy when it’s phrased as “feeding our good bacteria,” but this is more like wishful thinking. These fibers do feed our gut bacteria, but they feed the bad ones in addition to the good ones.

This isn’t a problem if our gut function and microbiome composition are optimal. But, if they aren’t optimal, which is extraordinarily common in modern times, this will exacerbate any gut dysfunction that’s going on.

(Fun fact: the gas that’s commonly associated with eating beans is a product of a suboptimal microbiome consuming soluble fiber)

On the other hand, the ability for insoluble fibers to move food through our gut is beneficial because gut motility is important for healthy gut function. But, this is a relatively trivial benefit in the context of grain consumption.

 

Grains, Legumes, and (Anti)nutrients

Whole grains, pseudograins, and legumes are touted for their nutrient content, specifically their vitamins, minerals, and protein. But when we consider their antinutrient content, their nutrient value is really pretty poor.

As I mentioned earlier, grains, pseudograins, and legumes are seeds. Seeds are an extraordinarily important part of plants – they’re needed for plants to reproduce. The nutrients in seeds aren’t meant for us, they’re meant to be used for growing a new plant.

Plants can’t protect their valuable seeds by running from predators or attacking them with sharp claws or teeth. Instead, their seeds have chemical defenses – compounds that protect their nutrients and cause harm to animals who eat them. These compounds are commonly referred to as antinutrients.

There are several types of antinutrients, including lectins, phytic acid (phytates), oxalic acid (oxalates), enzyme inhibitors, and saponins, each with unique harmful effects.

Lectins

Lectins are probably the most damaging and well-known antinutrients. You’ve probably heard of the most infamous lectin, gluten. Lectins inhibit nutrient absorption, cause bacterial overgrowth and systemic stress and inflammation, and damage our gut barrier, causing it to become permeable or “leaky” (2, 3, 4, 5, 6).

Gut permeability, or “leakiness,” allows undigested food particles and toxins to travel directly into the bloodstream, which can impair energy production and contribute to stress and inflammation (7, 8).

Phytic Acid and Oxalic Acid

Phytic acid and oxalic acid bind with calcium, magnesium, zinc, copper, potassium, iron, and other minerals, blocking their digestion and absorption in our guts and inhibiting our ability to use them (9, 10, 11). These minerals are vital for many processes, one of the most noteworthy being energy production.

Enzyme Inhibitors

Enzyme inhibitors block the enzymes in our guts that digest protein and starch, which prevents the digestion and absorption of protein and starches in the grains, pseudograins, and legumes, as well as in other foods we happen to be eating with them (9, 12, 13). Phytic acid also blocks some of these enzymes, further inhibiting the digestion of protein and starch (14, 15).

Saponins

Saponins, which are found mostly in pseudograins and legumes, inhibit protein-digesting enzymes, inhibit thyroid function (the regulator of our metabolism), and bind with and lower cholesterol (this isn’t beneficial, as we might be led to believe – I explain why here) (16, 17, 18).

 

Antinutrients No More

Somehow, the mainstream has found ways to spin the harmful effects of antinutrients into benefits. Impairing energy production and contributing to inflammation is considered “boosting immune function,” impairing starch digestion is considered “managing blood sugar,” and reducing cholesterol is, well, just reducing cholesterol, but this isn’t beneficial like we’ve been told.

If you ask me, it’s pretty clear that whole grains and legumes aren’t the health foods they’ve been made out to be. If anything, they appear to be worse than their obesity-, diabetes-, and heart disease-causing counterparts, refined grains. And this isn’t to mention the pesticides and GMOs that are ubiquitous among these crops.

But, it’s not all bad. In fact, grains and legumes can be prepared in ways that negate many of their negative effects. Cooking can deactivate a few of the antinutrients in these foods, but the traditional preparations of soaking, sprouting, and fermenting significantly reduce their antinutrient content, and may even alter their fiber composition (9, 19).

But if that doesn’t suit your fancy, you can skip these foods altogether!

Grains are most certainly not a necessary part of a healthy diet like they’ve been made out to be. Fruits and starch-containing foods that aren’t grains, including roots (carrots, yuca, turnips, etc.), tubers (potatoes and sweet potatoes), and vegetables in the gourd family (like squash and zucchini), are all great sources of carbohydrates with few antinutrients, if any.

(Note: some of these foods, like potatoes, do have antinutrients. But, they’re housed in the skins which can be easily removed.)

Also, while it is a grain, white rice is a relatively antinutrient-free carbohydrate source. This is because it’s stripped of its bran and hull, the parts of brown rice that contain most of the antinutrients.

Does all of this mean that if you eat any non-traditionally prepared grains, pseudograins, or legumes you can say goodbye to your health?

Of course not. But it does mean that their promotion as “health foods” is not supported, and we may want to reconsider how much of them we’re eating.

 

References

Grains and Legumes and Antinutrients, Oh My!

Despite the growing anti-grain movement, it’s still recommended that we consume 5-8 ounce equivalents or more of grains per day, and whole grains are still the face of the typical healthy diet (1).

Mainstream nutrition recommendations tell us that whole grains, pseudograins, and legumes are heart-healthy and promote a healthy weight. These food groups include foods like:

  • Wheat, corn, rye, barely, rice, millet, oats (grains)
  • Quinoa, amaranth, buckwheat (pseudograins)
  • Beans, soy, lentils, peanuts (legumes)

On the other hand, refined grains are the ones blamed for obesity, diabetes, and heart disease.

 

Holy Whole Grains vs. Evil Refined Grains

Let’s start with the basics.

Grains, pseudograins, and legumes are all seeds, which have 3 main components: bran, germ, and endosperm. The bran and germ contain most of the fiber and “nutrients,” and the endosperm is the carbohydrate-dense portion.

A whole grain is still intact – it contains all 3 of these components, while refined grains are stripped of the germ and bran, leaving only the endosperm.

So, the only difference between the “healthiest-of-all-foods” whole grains and the “inflammation-diabetes-obesity-and-heart-disease-causing” refined grains are the fiber and the “nutrients,” while the starch-containing endosperm is the same.

And, like whole grains, the “heart-healthy” pseudograins and legumes are full of fiber and “nutrients.”

But, it turns out that the fibers and “nutrients” found in these foods might not be so beneficial after all, leaving their supposed health-promoting effects in question.

 

Grains, Legumes, and Fiber

Whole grains, pseudograins, and legumes contain both soluble and insoluble fibers.

Soluble fibers are considered prebiotics because they feed our gut bacteria, whereas insoluble fibers are not digested by our gut bacteria and help to move food through our guts.

These fibers are considered beneficial because of ability to keep us full for longer, their prebiotic effects, and their colon cleansing effects.

But, these effects aren’t always so beneficial.

Keeping us full for longer might be favorable if we wanted to eat less, but eating less isn’t really beneficial unless we want to deprive ourselves of energy (Why “Eat Less and Exercise More” is the WORST Advice for Fat Loss and Health).

The ability for soluble fibers to feed our gut bacteria may sound healthy when it’s phrased as “feeding our good bacteria,” but this is more like wishful thinking. These fibers do feed our gut bacteria, but they feed the bad ones in addition to the good ones.

This isn’t a problem if our gut function and microbiome composition are optimal. But, if they aren’t optimal, which is extraordinarily common in modern times, this will exacerbate any gut dysfunction that’s going on.

(Fun fact: the gas that’s commonly associated with eating beans is a product of a suboptimal microbiome consuming soluble fiber)

On the other hand, the ability for insoluble fibers to move food through our gut is beneficial because gut motility is important for healthy gut function. But, this is a relatively trivial benefit in the context of grain consumption.

 

Grains, Legumes, and (Anti)nutrients

Whole grains, pseudograins, and legumes are touted for their nutrient content, specifically their vitamins, minerals, and protein. But when we consider their antinutrient content, their nutrient value is really pretty poor.

As I mentioned earlier, grains, pseudograins, and legumes are seeds. Seeds are an extraordinarily important part of plants – they’re needed for plants to reproduce. The nutrients in seeds aren’t meant for us, they’re meant to be used for growing a new plant.

Plants can’t protect their valuable seeds by running from predators or attacking them with sharp claws or teeth. Instead, their seeds have chemical defenses – compounds that protect their nutrients and cause harm to animals who eat them. These compounds are commonly referred to as antinutrients.

There are several types of antinutrients, including lectins, phytic acid (phytates), oxalic acid (oxalates), enzyme inhibitors, and saponins, each with unique harmful effects.

Lectins

Lectins are probably the most damaging and well-known antinutrients. You’ve probably heard of the most infamous lectin, gluten. Lectins inhibit nutrient absorption, cause bacterial overgrowth and systemic stress and inflammation, and damage our gut barrier, causing it to become permeable or “leaky” (2, 3, 4, 5, 6).

Gut permeability, or “leakiness,” allows undigested food particles and toxins to travel directly into the bloodstream, which can impair energy production and contribute to stress and inflammation (7, 8).

Phytic Acid and Oxalic Acid

Phytic acid and oxalic acid bind with calcium, magnesium, zinc, copper, potassium, iron, and other minerals, blocking their digestion and absorption in our guts and inhibiting our ability to use them (9, 10, 11). These minerals are vital for many processes, one of the most noteworthy being energy production.

Enzyme Inhibitors

Enzyme inhibitors block the enzymes in our guts that digest protein and starch, which prevents the digestion and absorption of protein and starches in the grains, pseudograins, and legumes, as well as in other foods we happen to be eating with them (9, 12, 13). Phytic acid also blocks some of these enzymes, further inhibiting the digestion of protein and starch (14, 15).

Saponins

Saponins, which are found mostly in pseudograins and legumes, inhibit protein-digesting enzymes, inhibit thyroid function (the regulator of our metabolism), and bind with and lower cholesterol (this isn’t beneficial, as we might be led to believe – I explain why here) (16, 17, 18).

 

Antinutrients No More

Somehow, the mainstream has found ways to spin the harmful effects of antinutrients into benefits. Impairing energy production and contributing to inflammation is considered “boosting immune function,” impairing starch digestion is considered “managing blood sugar,” and reducing cholesterol is, well, just reducing cholesterol, but this isn’t beneficial like we’ve been told.

If you ask me, it’s pretty clear that whole grains and legumes aren’t the health foods they’ve been made out to be. If anything, they appear to be worse than their obesity-, diabetes-, and heart disease-causing counterparts, refined grains. And this isn’t to mention the pesticides and GMOs that are ubiquitous among these crops.

But, it’s not all bad. In fact, grains and legumes can be prepared in ways that negate many of their negative effects. Cooking can deactivate a few of the antinutrients in these foods, but the traditional preparations of soaking, sprouting, and fermenting significantly reduce their antinutrient content, and may even alter their fiber composition (9, 19).

But if that doesn’t suit your fancy, you can skip these foods altogether!

Grains are most certainly not a necessary part of a healthy diet like they’ve been made out to be. Fruits and starch-containing foods that aren’t grains, including roots (carrots, yuca, turnips, etc.), tubers (potatoes and sweet potatoes), and vegetables in the gourd family (like squash and zucchini), are all great sources of carbohydrates with few antinutrients, if any.

(Note: some of these foods, like potatoes, do have antinutrients. But, they’re housed in the skins which can be easily removed.)

Also, while it is a grain, white rice is a relatively antinutrient-free carbohydrate source. This is because it’s stripped of its bran and hull, the parts of brown rice that contain most of the antinutrients.

Does all of this mean that if you eat any non-traditionally prepared grains, pseudograins, or legumes you can say goodbye to your health?

Of course not. But it does mean that their promotion as “health foods” is not supported, and we may want to reconsider how much of them we’re eating.

 

References

Grains and Legumes and Antinutrients, Oh My!

Despite the growing anti-grain movement, it’s still recommended that we consume 5-8 ounce equivalents or more of grains per day, and whole grains are still the face of the typical healthy diet (1).

Mainstream nutrition recommendations tell us that whole grains, pseudograins, and legumes are heart-healthy and promote a healthy weight. These food groups include foods like:

  • Wheat, corn, rye, barely, rice, millet, oats (grains)
  • Quinoa, amaranth, buckwheat (pseudograins)
  • Beans, soy, lentils, peanuts (legumes)

On the other hand, refined grains are the ones blamed for obesity, diabetes, and heart disease.

 

Holy Whole Grains vs. Evil Refined Grains

Let’s start with the basics.

Grains, pseudograins, and legumes are all seeds, which have 3 main components: bran, germ, and endosperm. The bran and germ contain most of the fiber and “nutrients,” and the endosperm is the carbohydrate-dense portion.

A whole grain is still intact – it contains all 3 of these components, while refined grains are stripped of the germ and bran, leaving only the endosperm.

So, the only difference between the “healthiest-of-all-foods” whole grains and the “inflammation-diabetes-obesity-and-heart-disease-causing” refined grains are the fiber and the “nutrients,” while the starch-containing endosperm is the same.

And, like whole grains, the “heart-healthy” pseudograins and legumes are full of fiber and “nutrients.”

But, it turns out that the fibers and “nutrients” found in these foods might not be so beneficial after all, leaving their supposed health-promoting effects in question.

 

Grains, Legumes, and Fiber

Whole grains, pseudograins, and legumes contain both soluble and insoluble fibers.

Soluble fibers are considered prebiotics because they feed our gut bacteria, whereas insoluble fibers are not digested by our gut bacteria and help to move food through our guts.

These fibers are considered beneficial because of ability to keep us full for longer, their prebiotic effects, and their colon cleansing effects.

But, these effects aren’t always so beneficial.

Keeping us full for longer might be favorable if we wanted to eat less, but eating less isn’t really beneficial unless we want to deprive ourselves of energy (Why “Eat Less and Exercise More” is the WORST Advice for Fat Loss and Health).

The ability for soluble fibers to feed our gut bacteria may sound healthy when it’s phrased as “feeding our good bacteria,” but this is more like wishful thinking. These fibers do feed our gut bacteria, but they feed the bad ones in addition to the good ones.

This isn’t a problem if our gut function and microbiome composition are optimal. But, if they aren’t optimal, which is extraordinarily common in modern times, this will exacerbate any gut dysfunction that’s going on.

(Fun fact: the gas that’s commonly associated with eating beans is a product of a suboptimal microbiome consuming soluble fiber)

On the other hand, the ability for insoluble fibers to move food through our gut is beneficial because gut motility is important for healthy gut function. But, this is a relatively trivial benefit in the context of grain consumption.

 

Grains, Legumes, and (Anti)nutrients

Whole grains, pseudograins, and legumes are touted for their nutrient content, specifically their vitamins, minerals, and protein. But when we consider their antinutrient content, their nutrient value is really pretty poor.

As I mentioned earlier, grains, pseudograins, and legumes are seeds. Seeds are an extraordinarily important part of plants – they’re needed for plants to reproduce. The nutrients in seeds aren’t meant for us, they’re meant to be used for growing a new plant.

Plants can’t protect their valuable seeds by running from predators or attacking them with sharp claws or teeth. Instead, their seeds have chemical defenses – compounds that protect their nutrients and cause harm to animals who eat them. These compounds are commonly referred to as antinutrients.

There are several types of antinutrients, including lectins, phytic acid (phytates), oxalic acid (oxalates), enzyme inhibitors, and saponins, each with unique harmful effects.

Lectins

Lectins are probably the most damaging and well-known antinutrients. You’ve probably heard of the most infamous lectin, gluten. Lectins inhibit nutrient absorption, cause bacterial overgrowth and systemic stress and inflammation, and damage our gut barrier, causing it to become permeable or “leaky” (2, 3, 4, 5, 6).

Gut permeability, or “leakiness,” allows undigested food particles and toxins to travel directly into the bloodstream, which can impair energy production and contribute to stress and inflammation (7, 8).

Phytic Acid and Oxalic Acid

Phytic acid and oxalic acid bind with calcium, magnesium, zinc, copper, potassium, iron, and other minerals, blocking their digestion and absorption in our guts and inhibiting our ability to use them (9, 10, 11). These minerals are vital for many processes, one of the most noteworthy being energy production.

Enzyme Inhibitors

Enzyme inhibitors block the enzymes in our guts that digest protein and starch, which prevents the digestion and absorption of protein and starches in the grains, pseudograins, and legumes, as well as in other foods we happen to be eating with them (9, 12, 13). Phytic acid also blocks some of these enzymes, further inhibiting the digestion of protein and starch (14, 15).

Saponins

Saponins, which are found mostly in pseudograins and legumes, inhibit protein-digesting enzymes, inhibit thyroid function (the regulator of our metabolism), and bind with and lower cholesterol (this isn’t beneficial, as we might be led to believe – I explain why here) (16, 17, 18).

 

Antinutrients No More

Somehow, the mainstream has found ways to spin the harmful effects of antinutrients into benefits. Impairing energy production and contributing to inflammation is considered “boosting immune function,” impairing starch digestion is considered “managing blood sugar,” and reducing cholesterol is, well, just reducing cholesterol, but this isn’t beneficial like we’ve been told.

If you ask me, it’s pretty clear that whole grains and legumes aren’t the health foods they’ve been made out to be. If anything, they appear to be worse than their obesity-, diabetes-, and heart disease-causing counterparts, refined grains. And this isn’t to mention the pesticides and GMOs that are ubiquitous among these crops.

But, it’s not all bad. In fact, grains and legumes can be prepared in ways that negate many of their negative effects. Cooking can deactivate a few of the antinutrients in these foods, but the traditional preparations of soaking, sprouting, and fermenting significantly reduce their antinutrient content, and may even alter their fiber composition (9, 19).

But if that doesn’t suit your fancy, you can skip these foods altogether!

Grains are most certainly not a necessary part of a healthy diet like they’ve been made out to be. Fruits and starch-containing foods that aren’t grains, including roots (carrots, yuca, turnips, etc.), tubers (potatoes and sweet potatoes), and vegetables in the gourd family (like squash and zucchini), are all great sources of carbohydrates with few antinutrients, if any.

(Note: some of these foods, like potatoes, do have antinutrients. But, they’re housed in the skins which can be easily removed.)

Also, while it is a grain, white rice is a relatively antinutrient-free carbohydrate source. This is because it’s stripped of its bran and hull, the parts of brown rice that contain most of the antinutrients.

Does all of this mean that if you eat any non-traditionally prepared grains, pseudograins, or legumes you can say goodbye to your health?

Of course not. But it does mean that their promotion as “health foods” is not supported, and we may want to reconsider how much of them we’re eating.

 

References

Grains and Legumes and Antinutrients, Oh My!

Despite the growing anti-grain movement, it’s still recommended that we consume 5-8 ounce equivalents or more of grains per day, and whole grains are still the face of the typical healthy diet (1).

Mainstream nutrition recommendations tell us that whole grains, pseudograins, and legumes are heart-healthy and promote a healthy weight. These food groups include foods like:

  • Wheat, corn, rye, barely, rice, millet, oats (grains)
  • Quinoa, amaranth, buckwheat (pseudograins)
  • Beans, soy, lentils, peanuts (legumes)

On the other hand, refined grains are the ones blamed for obesity, diabetes, and heart disease.

 

Holy Whole Grains vs. Evil Refined Grains

Let’s start with the basics.

Grains, pseudograins, and legumes are all seeds, which have 3 main components: bran, germ, and endosperm. The bran and germ contain most of the fiber and “nutrients,” and the endosperm is the carbohydrate-dense portion.

A whole grain is still intact – it contains all 3 of these components, while refined grains are stripped of the germ and bran, leaving only the endosperm.

So, the only difference between the “healthiest-of-all-foods” whole grains and the “inflammation-diabetes-obesity-and-heart-disease-causing” refined grains are the fiber and the “nutrients,” while the starch-containing endosperm is the same.

And, like whole grains, the “heart-healthy” pseudograins and legumes are full of fiber and “nutrients.”

But, it turns out that the fibers and “nutrients” found in these foods might not be so beneficial after all, leaving their supposed health-promoting effects in question.

 

Grains, Legumes, and Fiber

Whole grains, pseudograins, and legumes contain both soluble and insoluble fibers.

Soluble fibers are considered prebiotics because they feed our gut bacteria, whereas insoluble fibers are not digested by our gut bacteria and help to move food through our guts.

These fibers are considered beneficial because of ability to keep us full for longer, their prebiotic effects, and their colon cleansing effects.

But, these effects aren’t always so beneficial.

Keeping us full for longer might be favorable if we wanted to eat less, but eating less isn’t really beneficial unless we want to deprive ourselves of energy (Why “Eat Less and Exercise More” is the WORST Advice for Fat Loss and Health).

The ability for soluble fibers to feed our gut bacteria may sound healthy when it’s phrased as “feeding our good bacteria,” but this is more like wishful thinking. These fibers do feed our gut bacteria, but they feed the bad ones in addition to the good ones.

This isn’t a problem if our gut function and microbiome composition are optimal. But, if they aren’t optimal, which is extraordinarily common in modern times, this will exacerbate any gut dysfunction that’s going on.

(Fun fact: the gas that’s commonly associated with eating beans is a product of a suboptimal microbiome consuming soluble fiber)

On the other hand, the ability for insoluble fibers to move food through our gut is beneficial because gut motility is important for healthy gut function. But, this is a relatively trivial benefit in the context of grain consumption.

 

Grains, Legumes, and (Anti)nutrients

Whole grains, pseudograins, and legumes are touted for their nutrient content, specifically their vitamins, minerals, and protein. But when we consider their antinutrient content, their nutrient value is really pretty poor.

As I mentioned earlier, grains, pseudograins, and legumes are seeds. Seeds are an extraordinarily important part of plants – they’re needed for plants to reproduce. The nutrients in seeds aren’t meant for us, they’re meant to be used for growing a new plant.

Plants can’t protect their valuable seeds by running from predators or attacking them with sharp claws or teeth. Instead, their seeds have chemical defenses – compounds that protect their nutrients and cause harm to animals who eat them. These compounds are commonly referred to as antinutrients.

There are several types of antinutrients, including lectins, phytic acid (phytates), oxalic acid (oxalates), enzyme inhibitors, and saponins, each with unique harmful effects.

Lectins

Lectins are probably the most damaging and well-known antinutrients. You’ve probably heard of the most infamous lectin, gluten. Lectins inhibit nutrient absorption, cause bacterial overgrowth and systemic stress and inflammation, and damage our gut barrier, causing it to become permeable or “leaky” (2, 3, 4, 5, 6).

Gut permeability, or “leakiness,” allows undigested food particles and toxins to travel directly into the bloodstream, which can impair energy production and contribute to stress and inflammation (7, 8).

Phytic Acid and Oxalic Acid

Phytic acid and oxalic acid bind with calcium, magnesium, zinc, copper, potassium, iron, and other minerals, blocking their digestion and absorption in our guts and inhibiting our ability to use them (9, 10, 11). These minerals are vital for many processes, one of the most noteworthy being energy production.

Enzyme Inhibitors

Enzyme inhibitors block the enzymes in our guts that digest protein and starch, which prevents the digestion and absorption of protein and starches in the grains, pseudograins, and legumes, as well as in other foods we happen to be eating with them (9, 12, 13). Phytic acid also blocks some of these enzymes, further inhibiting the digestion of protein and starch (14, 15).

Saponins

Saponins, which are found mostly in pseudograins and legumes, inhibit protein-digesting enzymes, inhibit thyroid function (the regulator of our metabolism), and bind with and lower cholesterol (this isn’t beneficial, as we might be led to believe – I explain why here) (16, 17, 18).

 

Antinutrients No More

Somehow, the mainstream has found ways to spin the harmful effects of antinutrients into benefits. Impairing energy production and contributing to inflammation is considered “boosting immune function,” impairing starch digestion is considered “managing blood sugar,” and reducing cholesterol is, well, just reducing cholesterol, but this isn’t beneficial like we’ve been told.

If you ask me, it’s pretty clear that whole grains and legumes aren’t the health foods they’ve been made out to be. If anything, they appear to be worse than their obesity-, diabetes-, and heart disease-causing counterparts, refined grains. And this isn’t to mention the pesticides and GMOs that are ubiquitous among these crops.

But, it’s not all bad. In fact, grains and legumes can be prepared in ways that negate many of their negative effects. Cooking can deactivate a few of the antinutrients in these foods, but the traditional preparations of soaking, sprouting, and fermenting significantly reduce their antinutrient content, and may even alter their fiber composition (9, 19).

But if that doesn’t suit your fancy, you can skip these foods altogether!

Grains are most certainly not a necessary part of a healthy diet like they’ve been made out to be. Fruits and starch-containing foods that aren’t grains, including roots (carrots, yuca, turnips, etc.), tubers (potatoes and sweet potatoes), and vegetables in the gourd family (like squash and zucchini), are all great sources of carbohydrates with few antinutrients, if any.

(Note: some of these foods, like potatoes, do have antinutrients. But, they’re housed in the skins which can be easily removed.)

Also, while it is a grain, white rice is a relatively antinutrient-free carbohydrate source. This is because it’s stripped of its bran and hull, the parts of brown rice that contain most of the antinutrients.

Does all of this mean that if you eat any non-traditionally prepared grains, pseudograins, or legumes you can say goodbye to your health?

Of course not. But it does mean that their promotion as “health foods” is not supported, and we may want to reconsider how much of them we’re eating.

 

References

Grains and Legumes and Antinutrients, Oh My!

Despite the growing anti-grain movement, it’s still recommended that we consume 5-8 ounce equivalents or more of grains per day, and whole grains are still the face of the typical healthy diet (1).

Mainstream nutrition recommendations tell us that whole grains, pseudograins, and legumes are heart-healthy and promote a healthy weight. These food groups include foods like:

  • Wheat, corn, rye, barely, rice, millet, oats (grains)
  • Quinoa, amaranth, buckwheat (pseudograins)
  • Beans, soy, lentils, peanuts (legumes)

On the other hand, refined grains are the ones blamed for obesity, diabetes, and heart disease.

 

Holy Whole Grains vs. Evil Refined Grains

Let’s start with the basics.

Grains, pseudograins, and legumes are all seeds, which have 3 main components: bran, germ, and endosperm. The bran and germ contain most of the fiber and “nutrients,” and the endosperm is the carbohydrate-dense portion.

A whole grain is still intact – it contains all 3 of these components, while refined grains are stripped of the germ and bran, leaving only the endosperm.

So, the only difference between the “healthiest-of-all-foods” whole grains and the “inflammation-diabetes-obesity-and-heart-disease-causing” refined grains are the fiber and the “nutrients,” while the starch-containing endosperm is the same.

And, like whole grains, the “heart-healthy” pseudograins and legumes are full of fiber and “nutrients.”

But, it turns out that the fibers and “nutrients” found in these foods might not be so beneficial after all, leaving their supposed health-promoting effects in question.

 

Grains, Legumes, and Fiber

Whole grains, pseudograins, and legumes contain both soluble and insoluble fibers.

Soluble fibers are considered prebiotics because they feed our gut bacteria, whereas insoluble fibers are not digested by our gut bacteria and help to move food through our guts.

These fibers are considered beneficial because of ability to keep us full for longer, their prebiotic effects, and their colon cleansing effects.

But, these effects aren’t always so beneficial.

Keeping us full for longer might be favorable if we wanted to eat less, but eating less isn’t really beneficial unless we want to deprive ourselves of energy (Why “Eat Less and Exercise More” is the WORST Advice for Fat Loss and Health).

The ability for soluble fibers to feed our gut bacteria may sound healthy when it’s phrased as “feeding our good bacteria,” but this is more like wishful thinking. These fibers do feed our gut bacteria, but they feed the bad ones in addition to the good ones.

This isn’t a problem if our gut function and microbiome composition are optimal. But, if they aren’t optimal, which is extraordinarily common in modern times, this will exacerbate any gut dysfunction that’s going on.

(Fun fact: the gas that’s commonly associated with eating beans is a product of a suboptimal microbiome consuming soluble fiber)

On the other hand, the ability for insoluble fibers to move food through our gut is beneficial because gut motility is important for healthy gut function. But, this is a relatively trivial benefit in the context of grain consumption.

 

Grains, Legumes, and (Anti)nutrients

Whole grains, pseudograins, and legumes are touted for their nutrient content, specifically their vitamins, minerals, and protein. But when we consider their antinutrient content, their nutrient value is really pretty poor.

As I mentioned earlier, grains, pseudograins, and legumes are seeds. Seeds are an extraordinarily important part of plants – they’re needed for plants to reproduce. The nutrients in seeds aren’t meant for us, they’re meant to be used for growing a new plant.

Plants can’t protect their valuable seeds by running from predators or attacking them with sharp claws or teeth. Instead, their seeds have chemical defenses – compounds that protect their nutrients and cause harm to animals who eat them. These compounds are commonly referred to as antinutrients.

There are several types of antinutrients, including lectins, phytic acid (phytates), oxalic acid (oxalates), enzyme inhibitors, and saponins, each with unique harmful effects.

Lectins

Lectins are probably the most damaging and well-known antinutrients. You’ve probably heard of the most infamous lectin, gluten. Lectins inhibit nutrient absorption, cause bacterial overgrowth and systemic stress and inflammation, and damage our gut barrier, causing it to become permeable or “leaky” (2, 3, 4, 5, 6).

Gut permeability, or “leakiness,” allows undigested food particles and toxins to travel directly into the bloodstream, which can impair energy production and contribute to stress and inflammation (7, 8).

Phytic Acid and Oxalic Acid

Phytic acid and oxalic acid bind with calcium, magnesium, zinc, copper, potassium, iron, and other minerals, blocking their digestion and absorption in our guts and inhibiting our ability to use them (9, 10, 11). These minerals are vital for many processes, one of the most noteworthy being energy production.

Enzyme Inhibitors

Enzyme inhibitors block the enzymes in our guts that digest protein and starch, which prevents the digestion and absorption of protein and starches in the grains, pseudograins, and legumes, as well as in other foods we happen to be eating with them (9, 12, 13). Phytic acid also blocks some of these enzymes, further inhibiting the digestion of protein and starch (14, 15).

Saponins

Saponins, which are found mostly in pseudograins and legumes, inhibit protein-digesting enzymes, inhibit thyroid function (the regulator of our metabolism), and bind with and lower cholesterol (this isn’t beneficial, as we might be led to believe – I explain why here) (16, 17, 18).

 

Antinutrients No More

Somehow, the mainstream has found ways to spin the harmful effects of antinutrients into benefits. Impairing energy production and contributing to inflammation is considered “boosting immune function,” impairing starch digestion is considered “managing blood sugar,” and reducing cholesterol is, well, just reducing cholesterol, but this isn’t beneficial like we’ve been told.

If you ask me, it’s pretty clear that whole grains and legumes aren’t the health foods they’ve been made out to be. If anything, they appear to be worse than their obesity-, diabetes-, and heart disease-causing counterparts, refined grains. And this isn’t to mention the pesticides and GMOs that are ubiquitous among these crops.

But, it’s not all bad. In fact, grains and legumes can be prepared in ways that negate many of their negative effects. Cooking can deactivate a few of the antinutrients in these foods, but the traditional preparations of soaking, sprouting, and fermenting significantly reduce their antinutrient content, and may even alter their fiber composition (9, 19).

But if that doesn’t suit your fancy, you can skip these foods altogether!

Grains are most certainly not a necessary part of a healthy diet like they’ve been made out to be. Fruits and starch-containing foods that aren’t grains, including roots (carrots, yuca, turnips, etc.), tubers (potatoes and sweet potatoes), and vegetables in the gourd family (like squash and zucchini), are all great sources of carbohydrates with few antinutrients, if any.

(Note: some of these foods, like potatoes, do have antinutrients. But, they’re housed in the skins which can be easily removed.)

Also, while it is a grain, white rice is a relatively antinutrient-free carbohydrate source. This is because it’s stripped of its bran and hull, the parts of brown rice that contain most of the antinutrients.

Does all of this mean that if you eat any non-traditionally prepared grains, pseudograins, or legumes you can say goodbye to your health?

Of course not. But it does mean that their promotion as “health foods” is not supported, and we may want to reconsider how much of them we’re eating.

 

References

Grains and Legumes and Antinutrients, Oh My!

Despite the growing anti-grain movement, it’s still recommended that we consume 5-8 ounce equivalents or more of grains per day, and whole grains are still the face of the typical healthy diet (1).

Mainstream nutrition recommendations tell us that whole grains, pseudograins, and legumes are heart-healthy and promote a healthy weight. These food groups include foods like:

  • Wheat, corn, rye, barely, rice, millet, oats (grains)
  • Quinoa, amaranth, buckwheat (pseudograins)
  • Beans, soy, lentils, peanuts (legumes)

On the other hand, refined grains are the ones blamed for obesity, diabetes, and heart disease.

 

Holy Whole Grains vs. Evil Refined Grains

Let’s start with the basics.

Grains, pseudograins, and legumes are all seeds, which have 3 main components: bran, germ, and endosperm. The bran and germ contain most of the fiber and “nutrients,” and the endosperm is the carbohydrate-dense portion.

A whole grain is still intact – it contains all 3 of these components, while refined grains are stripped of the germ and bran, leaving only the endosperm.

So, the only difference between the “healthiest-of-all-foods” whole grains and the “inflammation-diabetes-obesity-and-heart-disease-causing” refined grains are the fiber and the “nutrients,” while the starch-containing endosperm is the same.

And, like whole grains, the “heart-healthy” pseudograins and legumes are full of fiber and “nutrients.”

But, it turns out that the fibers and “nutrients” found in these foods might not be so beneficial after all, leaving their supposed health-promoting effects in question.

 

Grains, Legumes, and Fiber

Whole grains, pseudograins, and legumes contain both soluble and insoluble fibers.

Soluble fibers are considered prebiotics because they feed our gut bacteria, whereas insoluble fibers are not digested by our gut bacteria and help to move food through our guts.

These fibers are considered beneficial because of ability to keep us full for longer, their prebiotic effects, and their colon cleansing effects.

But, these effects aren’t always so beneficial.

Keeping us full for longer might be favorable if we wanted to eat less, but eating less isn’t really beneficial unless we want to deprive ourselves of energy (Why “Eat Less and Exercise More” is the WORST Advice for Fat Loss and Health).

The ability for soluble fibers to feed our gut bacteria may sound healthy when it’s phrased as “feeding our good bacteria,” but this is more like wishful thinking. These fibers do feed our gut bacteria, but they feed the bad ones in addition to the good ones.

This isn’t a problem if our gut function and microbiome composition are optimal. But, if they aren’t optimal, which is extraordinarily common in modern times, this will exacerbate any gut dysfunction that’s going on.

(Fun fact: the gas that’s commonly associated with eating beans is a product of a suboptimal microbiome consuming soluble fiber)

On the other hand, the ability for insoluble fibers to move food through our gut is beneficial because gut motility is important for healthy gut function. But, this is a relatively trivial benefit in the context of grain consumption.

 

Grains, Legumes, and (Anti)nutrients

Whole grains, pseudograins, and legumes are touted for their nutrient content, specifically their vitamins, minerals, and protein. But when we consider their antinutrient content, their nutrient value is really pretty poor.

As I mentioned earlier, grains, pseudograins, and legumes are seeds. Seeds are an extraordinarily important part of plants – they’re needed for plants to reproduce. The nutrients in seeds aren’t meant for us, they’re meant to be used for growing a new plant.

Plants can’t protect their valuable seeds by running from predators or attacking them with sharp claws or teeth. Instead, their seeds have chemical defenses – compounds that protect their nutrients and cause harm to animals who eat them. These compounds are commonly referred to as antinutrients.

There are several types of antinutrients, including lectins, phytic acid (phytates), oxalic acid (oxalates), enzyme inhibitors, and saponins, each with unique harmful effects.

Lectins

Lectins are probably the most damaging and well-known antinutrients. You’ve probably heard of the most infamous lectin, gluten. Lectins inhibit nutrient absorption, cause bacterial overgrowth and systemic stress and inflammation, and damage our gut barrier, causing it to become permeable or “leaky” (2, 3, 4, 5, 6).

Gut permeability, or “leakiness,” allows undigested food particles and toxins to travel directly into the bloodstream, which can impair energy production and contribute to stress and inflammation (7, 8).

Phytic Acid and Oxalic Acid

Phytic acid and oxalic acid bind with calcium, magnesium, zinc, copper, potassium, iron, and other minerals, blocking their digestion and absorption in our guts and inhibiting our ability to use them (9, 10, 11). These minerals are vital for many processes, one of the most noteworthy being energy production.

Enzyme Inhibitors

Enzyme inhibitors block the enzymes in our guts that digest protein and starch, which prevents the digestion and absorption of protein and starches in the grains, pseudograins, and legumes, as well as in other foods we happen to be eating with them (9, 12, 13). Phytic acid also blocks some of these enzymes, further inhibiting the digestion of protein and starch (14, 15).

Saponins

Saponins, which are found mostly in pseudograins and legumes, inhibit protein-digesting enzymes, inhibit thyroid function (the regulator of our metabolism), and bind with and lower cholesterol (this isn’t beneficial, as we might be led to believe – I explain why here) (16, 17, 18).

 

Antinutrients No More

Somehow, the mainstream has found ways to spin the harmful effects of antinutrients into benefits. Impairing energy production and contributing to inflammation is considered “boosting immune function,” impairing starch digestion is considered “managing blood sugar,” and reducing cholesterol is, well, just reducing cholesterol, but this isn’t beneficial like we’ve been told.

If you ask me, it’s pretty clear that whole grains and legumes aren’t the health foods they’ve been made out to be. If anything, they appear to be worse than their obesity-, diabetes-, and heart disease-causing counterparts, refined grains. And this isn’t to mention the pesticides and GMOs that are ubiquitous among these crops.

But, it’s not all bad. In fact, grains and legumes can be prepared in ways that negate many of their negative effects. Cooking can deactivate a few of the antinutrients in these foods, but the traditional preparations of soaking, sprouting, and fermenting significantly reduce their antinutrient content, and may even alter their fiber composition (9, 19).

But if that doesn’t suit your fancy, you can skip these foods altogether!

Grains are most certainly not a necessary part of a healthy diet like they’ve been made out to be. Fruits and starch-containing foods that aren’t grains, including roots (carrots, yuca, turnips, etc.), tubers (potatoes and sweet potatoes), and vegetables in the gourd family (like squash and zucchini), are all great sources of carbohydrates with few antinutrients, if any.

(Note: some of these foods, like potatoes, do have antinutrients. But, they’re housed in the skins which can be easily removed.)

Also, while it is a grain, white rice is a relatively antinutrient-free carbohydrate source. This is because it’s stripped of its bran and hull, the parts of brown rice that contain most of the antinutrients.

Does all of this mean that if you eat any non-traditionally prepared grains, pseudograins, or legumes you can say goodbye to your health?

Of course not. But it does mean that their promotion as “health foods” is not supported, and we may want to reconsider how much of them we’re eating.

 

References

Grains and Legumes and Antinutrients, Oh My!

Despite the growing anti-grain movement, it’s still recommended that we consume 5-8 ounce equivalents or more of grains per day, and whole grains are still the face of the typical healthy diet (1).

Mainstream nutrition recommendations tell us that whole grains, pseudograins, and legumes are heart-healthy and promote a healthy weight. These food groups include foods like:

  • Wheat, corn, rye, barely, rice, millet, oats (grains)
  • Quinoa, amaranth, buckwheat (pseudograins)
  • Beans, soy, lentils, peanuts (legumes)

On the other hand, refined grains are the ones blamed for obesity, diabetes, and heart disease.

 

Holy Whole Grains vs. Evil Refined Grains

Let’s start with the basics.

Grains, pseudograins, and legumes are all seeds, which have 3 main components: bran, germ, and endosperm. The bran and germ contain most of the fiber and “nutrients,” and the endosperm is the carbohydrate-dense portion.

A whole grain is still intact – it contains all 3 of these components, while refined grains are stripped of the germ and bran, leaving only the endosperm.

So, the only difference between the “healthiest-of-all-foods” whole grains and the “inflammation-diabetes-obesity-and-heart-disease-causing” refined grains are the fiber and the “nutrients,” while the starch-containing endosperm is the same.

And, like whole grains, the “heart-healthy” pseudograins and legumes are full of fiber and “nutrients.”

But, it turns out that the fibers and “nutrients” found in these foods might not be so beneficial after all, leaving their supposed health-promoting effects in question.

 

Grains, Legumes, and Fiber

Whole grains, pseudograins, and legumes contain both soluble and insoluble fibers.

Soluble fibers are considered prebiotics because they feed our gut bacteria, whereas insoluble fibers are not digested by our gut bacteria and help to move food through our guts.

These fibers are considered beneficial because of ability to keep us full for longer, their prebiotic effects, and their colon cleansing effects.

But, these effects aren’t always so beneficial.

Keeping us full for longer might be favorable if we wanted to eat less, but eating less isn’t really beneficial unless we want to deprive ourselves of energy (Why “Eat Less and Exercise More” is the WORST Advice for Fat Loss and Health).

The ability for soluble fibers to feed our gut bacteria may sound healthy when it’s phrased as “feeding our good bacteria,” but this is more like wishful thinking. These fibers do feed our gut bacteria, but they feed the bad ones in addition to the good ones.

This isn’t a problem if our gut function and microbiome composition are optimal. But, if they aren’t optimal, which is extraordinarily common in modern times, this will exacerbate any gut dysfunction that’s going on.

(Fun fact: the gas that’s commonly associated with eating beans is a product of a suboptimal microbiome consuming soluble fiber)

On the other hand, the ability for insoluble fibers to move food through our gut is beneficial because gut motility is important for healthy gut function. But, this is a relatively trivial benefit in the context of grain consumption.

 

Grains, Legumes, and (Anti)nutrients

Whole grains, pseudograins, and legumes are touted for their nutrient content, specifically their vitamins, minerals, and protein. But when we consider their antinutrient content, their nutrient value is really pretty poor.

As I mentioned earlier, grains, pseudograins, and legumes are seeds. Seeds are an extraordinarily important part of plants – they’re needed for plants to reproduce. The nutrients in seeds aren’t meant for us, they’re meant to be used for growing a new plant.

Plants can’t protect their valuable seeds by running from predators or attacking them with sharp claws or teeth. Instead, their seeds have chemical defenses – compounds that protect their nutrients and cause harm to animals who eat them. These compounds are commonly referred to as antinutrients.

There are several types of antinutrients, including lectins, phytic acid (phytates), oxalic acid (oxalates), enzyme inhibitors, and saponins, each with unique harmful effects.

Lectins

Lectins are probably the most damaging and well-known antinutrients. You’ve probably heard of the most infamous lectin, gluten. Lectins inhibit nutrient absorption, cause bacterial overgrowth and systemic stress and inflammation, and damage our gut barrier, causing it to become permeable or “leaky” (2, 3, 4, 5, 6).

Gut permeability, or “leakiness,” allows undigested food particles and toxins to travel directly into the bloodstream, which can impair energy production and contribute to stress and inflammation (7, 8).

Phytic Acid and Oxalic Acid

Phytic acid and oxalic acid bind with calcium, magnesium, zinc, copper, potassium, iron, and other minerals, blocking their digestion and absorption in our guts and inhibiting our ability to use them (9, 10, 11). These minerals are vital for many processes, one of the most noteworthy being energy production.

Enzyme Inhibitors

Enzyme inhibitors block the enzymes in our guts that digest protein and starch, which prevents the digestion and absorption of protein and starches in the grains, pseudograins, and legumes, as well as in other foods we happen to be eating with them (9, 12, 13). Phytic acid also blocks some of these enzymes, further inhibiting the digestion of protein and starch (14, 15).

Saponins

Saponins, which are found mostly in pseudograins and legumes, inhibit protein-digesting enzymes, inhibit thyroid function (the regulator of our metabolism), and bind with and lower cholesterol (this isn’t beneficial, as we might be led to believe – I explain why here) (16, 17, 18).

 

Antinutrients No More

Somehow, the mainstream has found ways to spin the harmful effects of antinutrients into benefits. Impairing energy production and contributing to inflammation is considered “boosting immune function,” impairing starch digestion is considered “managing blood sugar,” and reducing cholesterol is, well, just reducing cholesterol, but this isn’t beneficial like we’ve been told.

If you ask me, it’s pretty clear that whole grains and legumes aren’t the health foods they’ve been made out to be. If anything, they appear to be worse than their obesity-, diabetes-, and heart disease-causing counterparts, refined grains. And this isn’t to mention the pesticides and GMOs that are ubiquitous among these crops.

But, it’s not all bad. In fact, grains and legumes can be prepared in ways that negate many of their negative effects. Cooking can deactivate a few of the antinutrients in these foods, but the traditional preparations of soaking, sprouting, and fermenting significantly reduce their antinutrient content, and may even alter their fiber composition (9, 19).

But if that doesn’t suit your fancy, you can skip these foods altogether!

Grains are most certainly not a necessary part of a healthy diet like they’ve been made out to be. Fruits and starch-containing foods that aren’t grains, including roots (carrots, yuca, turnips, etc.), tubers (potatoes and sweet potatoes), and vegetables in the gourd family (like squash and zucchini), are all great sources of carbohydrates with few antinutrients, if any.

(Note: some of these foods, like potatoes, do have antinutrients. But, they’re housed in the skins which can be easily removed.)

Also, while it is a grain, white rice is a relatively antinutrient-free carbohydrate source. This is because it’s stripped of its bran and hull, the parts of brown rice that contain most of the antinutrients.

Does all of this mean that if you eat any non-traditionally prepared grains, pseudograins, or legumes you can say goodbye to your health?

Of course not. But it does mean that their promotion as “health foods” is not supported, and we may want to reconsider how much of them we’re eating.

 

References

Grains and Legumes and Antinutrients, Oh My!

Despite the growing anti-grain movement, it’s still recommended that we consume 5-8 ounce equivalents or more of grains per day, and whole grains are still the face of the typical healthy diet (1).

Mainstream nutrition recommendations tell us that whole grains, pseudograins, and legumes are heart-healthy and promote a healthy weight. These food groups include foods like:

  • Wheat, corn, rye, barely, rice, millet, oats (grains)
  • Quinoa, amaranth, buckwheat (pseudograins)
  • Beans, soy, lentils, peanuts (legumes)

On the other hand, refined grains are the ones blamed for obesity, diabetes, and heart disease.

 

Holy Whole Grains vs. Evil Refined Grains

Let’s start with the basics.

Grains, pseudograins, and legumes are all seeds, which have 3 main components: bran, germ, and endosperm. The bran and germ contain most of the fiber and “nutrients,” and the endosperm is the carbohydrate-dense portion.

A whole grain is still intact – it contains all 3 of these components, while refined grains are stripped of the germ and bran, leaving only the endosperm.

So, the only difference between the “healthiest-of-all-foods” whole grains and the “inflammation-diabetes-obesity-and-heart-disease-causing” refined grains are the fiber and the “nutrients,” while the starch-containing endosperm is the same.

And, like whole grains, the “heart-healthy” pseudograins and legumes are full of fiber and “nutrients.”

But, it turns out that the fibers and “nutrients” found in these foods might not be so beneficial after all, leaving their supposed health-promoting effects in question.

 

Grains, Legumes, and Fiber

Whole grains, pseudograins, and legumes contain both soluble and insoluble fibers.

Soluble fibers are considered prebiotics because they feed our gut bacteria, whereas insoluble fibers are not digested by our gut bacteria and help to move food through our guts.

These fibers are considered beneficial because of ability to keep us full for longer, their prebiotic effects, and their colon cleansing effects.

But, these effects aren’t always so beneficial.

Keeping us full for longer might be favorable if we wanted to eat less, but eating less isn’t really beneficial unless we want to deprive ourselves of energy (Why “Eat Less and Exercise More” is the WORST Advice for Fat Loss and Health).

The ability for soluble fibers to feed our gut bacteria may sound healthy when it’s phrased as “feeding our good bacteria,” but this is more like wishful thinking. These fibers do feed our gut bacteria, but they feed the bad ones in addition to the good ones.

This isn’t a problem if our gut function and microbiome composition are optimal. But, if they aren’t optimal, which is extraordinarily common in modern times, this will exacerbate any gut dysfunction that’s going on.

(Fun fact: the gas that’s commonly associated with eating beans is a product of a suboptimal microbiome consuming soluble fiber)

On the other hand, the ability for insoluble fibers to move food through our gut is beneficial because gut motility is important for healthy gut function. But, this is a relatively trivial benefit in the context of grain consumption.

 

Grains, Legumes, and (Anti)nutrients

Whole grains, pseudograins, and legumes are touted for their nutrient content, specifically their vitamins, minerals, and protein. But when we consider their antinutrient content, their nutrient value is really pretty poor.

As I mentioned earlier, grains, pseudograins, and legumes are seeds. Seeds are an extraordinarily important part of plants – they’re needed for plants to reproduce. The nutrients in seeds aren’t meant for us, they’re meant to be used for growing a new plant.

Plants can’t protect their valuable seeds by running from predators or attacking them with sharp claws or teeth. Instead, their seeds have chemical defenses – compounds that protect their nutrients and cause harm to animals who eat them. These compounds are commonly referred to as antinutrients.

There are several types of antinutrients, including lectins, phytic acid (phytates), oxalic acid (oxalates), enzyme inhibitors, and saponins, each with unique harmful effects.

Lectins

Lectins are probably the most damaging and well-known antinutrients. You’ve probably heard of the most infamous lectin, gluten. Lectins inhibit nutrient absorption, cause bacterial overgrowth and systemic stress and inflammation, and damage our gut barrier, causing it to become permeable or “leaky” (2, 3, 4, 5, 6).

Gut permeability, or “leakiness,” allows undigested food particles and toxins to travel directly into the bloodstream, which can impair energy production and contribute to stress and inflammation (7, 8).

Phytic Acid and Oxalic Acid

Phytic acid and oxalic acid bind with calcium, magnesium, zinc, copper, potassium, iron, and other minerals, blocking their digestion and absorption in our guts and inhibiting our ability to use them (9, 10, 11). These minerals are vital for many processes, one of the most noteworthy being energy production.

Enzyme Inhibitors

Enzyme inhibitors block the enzymes in our guts that digest protein and starch, which prevents the digestion and absorption of protein and starches in the grains, pseudograins, and legumes, as well as in other foods we happen to be eating with them (9, 12, 13). Phytic acid also blocks some of these enzymes, further inhibiting the digestion of protein and starch (14, 15).

Saponins

Saponins, which are found mostly in pseudograins and legumes, inhibit protein-digesting enzymes, inhibit thyroid function (the regulator of our metabolism), and bind with and lower cholesterol (this isn’t beneficial, as we might be led to believe – I explain why here) (16, 17, 18).

 

Antinutrients No More

Somehow, the mainstream has found ways to spin the harmful effects of antinutrients into benefits. Impairing energy production and contributing to inflammation is considered “boosting immune function,” impairing starch digestion is considered “managing blood sugar,” and reducing cholesterol is, well, just reducing cholesterol, but this isn’t beneficial like we’ve been told.

If you ask me, it’s pretty clear that whole grains and legumes aren’t the health foods they’ve been made out to be. If anything, they appear to be worse than their obesity-, diabetes-, and heart disease-causing counterparts, refined grains. And this isn’t to mention the pesticides and GMOs that are ubiquitous among these crops.

But, it’s not all bad. In fact, grains and legumes can be prepared in ways that negate many of their negative effects. Cooking can deactivate a few of the antinutrients in these foods, but the traditional preparations of soaking, sprouting, and fermenting significantly reduce their antinutrient content, and may even alter their fiber composition (9, 19).

But if that doesn’t suit your fancy, you can skip these foods altogether!

Grains are most certainly not a necessary part of a healthy diet like they’ve been made out to be. Fruits and starch-containing foods that aren’t grains, including roots (carrots, yuca, turnips, etc.), tubers (potatoes and sweet potatoes), and vegetables in the gourd family (like squash and zucchini), are all great sources of carbohydrates with few antinutrients, if any.

(Note: some of these foods, like potatoes, do have antinutrients. But, they’re housed in the skins which can be easily removed.)

Also, while it is a grain, white rice is a relatively antinutrient-free carbohydrate source. This is because it’s stripped of its bran and hull, the parts of brown rice that contain most of the antinutrients.

Does all of this mean that if you eat any non-traditionally prepared grains, pseudograins, or legumes you can say goodbye to your health?

Of course not. But it does mean that their promotion as “health foods” is not supported, and we may want to reconsider how much of them we’re eating.

 

References

Grains and Legumes and Antinutrients, Oh My!

Despite the growing anti-grain movement, it’s still recommended that we consume 5-8 ounce equivalents or more of grains per day, and whole grains are still the face of the typical healthy diet (1).

Mainstream nutrition recommendations tell us that whole grains, pseudograins, and legumes are heart-healthy and promote a healthy weight. These food groups include foods like:

  • Wheat, corn, rye, barely, rice, millet, oats (grains)
  • Quinoa, amaranth, buckwheat (pseudograins)
  • Beans, soy, lentils, peanuts (legumes)

On the other hand, refined grains are the ones blamed for obesity, diabetes, and heart disease.

 

Holy Whole Grains vs. Evil Refined Grains

Let’s start with the basics.

Grains, pseudograins, and legumes are all seeds, which have 3 main components: bran, germ, and endosperm. The bran and germ contain most of the fiber and “nutrients,” and the endosperm is the carbohydrate-dense portion.

A whole grain is still intact – it contains all 3 of these components, while refined grains are stripped of the germ and bran, leaving only the endosperm.

So, the only difference between the “healthiest-of-all-foods” whole grains and the “inflammation-diabetes-obesity-and-heart-disease-causing” refined grains are the fiber and the “nutrients,” while the starch-containing endosperm is the same.

And, like whole grains, the “heart-healthy” pseudograins and legumes are full of fiber and “nutrients.”

But, it turns out that the fibers and “nutrients” found in these foods might not be so beneficial after all, leaving their supposed health-promoting effects in question.

 

Grains, Legumes, and Fiber

Whole grains, pseudograins, and legumes contain both soluble and insoluble fibers.

Soluble fibers are considered prebiotics because they feed our gut bacteria, whereas insoluble fibers are not digested by our gut bacteria and help to move food through our guts.

These fibers are considered beneficial because of ability to keep us full for longer, their prebiotic effects, and their colon cleansing effects.

But, these effects aren’t always so beneficial.

Keeping us full for longer might be favorable if we wanted to eat less, but eating less isn’t really beneficial unless we want to deprive ourselves of energy (Why “Eat Less and Exercise More” is the WORST Advice for Fat Loss and Health).

The ability for soluble fibers to feed our gut bacteria may sound healthy when it’s phrased as “feeding our good bacteria,” but this is more like wishful thinking. These fibers do feed our gut bacteria, but they feed the bad ones in addition to the good ones.

This isn’t a problem if our gut function and microbiome composition are optimal. But, if they aren’t optimal, which is extraordinarily common in modern times, this will exacerbate any gut dysfunction that’s going on.

(Fun fact: the gas that’s commonly associated with eating beans is a product of a suboptimal microbiome consuming soluble fiber)

On the other hand, the ability for insoluble fibers to move food through our gut is beneficial because gut motility is important for healthy gut function. But, this is a relatively trivial benefit in the context of grain consumption.

 

Grains, Legumes, and (Anti)nutrients

Whole grains, pseudograins, and legumes are touted for their nutrient content, specifically their vitamins, minerals, and protein. But when we consider their antinutrient content, their nutrient value is really pretty poor.

As I mentioned earlier, grains, pseudograins, and legumes are seeds. Seeds are an extraordinarily important part of plants – they’re needed for plants to reproduce. The nutrients in seeds aren’t meant for us, they’re meant to be used for growing a new plant.

Plants can’t protect their valuable seeds by running from predators or attacking them with sharp claws or teeth. Instead, their seeds have chemical defenses – compounds that protect their nutrients and cause harm to animals who eat them. These compounds are commonly referred to as antinutrients.

There are several types of antinutrients, including lectins, phytic acid (phytates), oxalic acid (oxalates), enzyme inhibitors, and saponins, each with unique harmful effects.

Lectins

Lectins are probably the most damaging and well-known antinutrients. You’ve probably heard of the most infamous lectin, gluten. Lectins inhibit nutrient absorption, cause bacterial overgrowth and systemic stress and inflammation, and damage our gut barrier, causing it to become permeable or “leaky” (2, 3, 4, 5, 6).

Gut permeability, or “leakiness,” allows undigested food particles and toxins to travel directly into the bloodstream, which can impair energy production and contribute to stress and inflammation (7, 8).

Phytic Acid and Oxalic Acid

Phytic acid and oxalic acid bind with calcium, magnesium, zinc, copper, potassium, iron, and other minerals, blocking their digestion and absorption in our guts and inhibiting our ability to use them (9, 10, 11). These minerals are vital for many processes, one of the most noteworthy being energy production.

Enzyme Inhibitors

Enzyme inhibitors block the enzymes in our guts that digest protein and starch, which prevents the digestion and absorption of protein and starches in the grains, pseudograins, and legumes, as well as in other foods we happen to be eating with them (9, 12, 13). Phytic acid also blocks some of these enzymes, further inhibiting the digestion of protein and starch (14, 15).

Saponins

Saponins, which are found mostly in pseudograins and legumes, inhibit protein-digesting enzymes, inhibit thyroid function (the regulator of our metabolism), and bind with and lower cholesterol (this isn’t beneficial, as we might be led to believe – I explain why here) (16, 17, 18).

 

Antinutrients No More

Somehow, the mainstream has found ways to spin the harmful effects of antinutrients into benefits. Impairing energy production and contributing to inflammation is considered “boosting immune function,” impairing starch digestion is considered “managing blood sugar,” and reducing cholesterol is, well, just reducing cholesterol, but this isn’t beneficial like we’ve been told.

If you ask me, it’s pretty clear that whole grains and legumes aren’t the health foods they’ve been made out to be. If anything, they appear to be worse than their obesity-, diabetes-, and heart disease-causing counterparts, refined grains. And this isn’t to mention the pesticides and GMOs that are ubiquitous among these crops.

But, it’s not all bad. In fact, grains and legumes can be prepared in ways that negate many of their negative effects. Cooking can deactivate a few of the antinutrients in these foods, but the traditional preparations of soaking, sprouting, and fermenting significantly reduce their antinutrient content, and may even alter their fiber composition (9, 19).

But if that doesn’t suit your fancy, you can skip these foods altogether!

Grains are most certainly not a necessary part of a healthy diet like they’ve been made out to be. Fruits and starch-containing foods that aren’t grains, including roots (carrots, yuca, turnips, etc.), tubers (potatoes and sweet potatoes), and vegetables in the gourd family (like squash and zucchini), are all great sources of carbohydrates with few antinutrients, if any.

(Note: some of these foods, like potatoes, do have antinutrients. But, they’re housed in the skins which can be easily removed.)

Also, while it is a grain, white rice is a relatively antinutrient-free carbohydrate source. This is because it’s stripped of its bran and hull, the parts of brown rice that contain most of the antinutrients.

Does all of this mean that if you eat any non-traditionally prepared grains, pseudograins, or legumes you can say goodbye to your health?

Of course not. But it does mean that their promotion as “health foods” is not supported, and we may want to reconsider how much of them we’re eating.

 

References

Grains and Legumes and Antinutrients, Oh My!

Despite the growing anti-grain movement, it’s still recommended that we consume 5-8 ounce equivalents or more of grains per day, and whole grains are still the face of the typical healthy diet (1).

Mainstream nutrition recommendations tell us that whole grains, pseudograins, and legumes are heart-healthy and promote a healthy weight. These food groups include foods like:

  • Wheat, corn, rye, barely, rice, millet, oats (grains)
  • Quinoa, amaranth, buckwheat (pseudograins)
  • Beans, soy, lentils, peanuts (legumes)

On the other hand, refined grains are the ones blamed for obesity, diabetes, and heart disease.

 

Holy Whole Grains vs. Evil Refined Grains

Let’s start with the basics.

Grains, pseudograins, and legumes are all seeds, which have 3 main components: bran, germ, and endosperm. The bran and germ contain most of the fiber and “nutrients,” and the endosperm is the carbohydrate-dense portion.

A whole grain is still intact – it contains all 3 of these components, while refined grains are stripped of the germ and bran, leaving only the endosperm.

So, the only difference between the “healthiest-of-all-foods” whole grains and the “inflammation-diabetes-obesity-and-heart-disease-causing” refined grains are the fiber and the “nutrients,” while the starch-containing endosperm is the same.

And, like whole grains, the “heart-healthy” pseudograins and legumes are full of fiber and “nutrients.”

But, it turns out that the fibers and “nutrients” found in these foods might not be so beneficial after all, leaving their supposed health-promoting effects in question.

 

Grains, Legumes, and Fiber

Whole grains, pseudograins, and legumes contain both soluble and insoluble fibers.

Soluble fibers are considered prebiotics because they feed our gut bacteria, whereas insoluble fibers are not digested by our gut bacteria and help to move food through our guts.

These fibers are considered beneficial because of ability to keep us full for longer, their prebiotic effects, and their colon cleansing effects.

But, these effects aren’t always so beneficial.

Keeping us full for longer might be favorable if we wanted to eat less, but eating less isn’t really beneficial unless we want to deprive ourselves of energy (Why “Eat Less and Exercise More” is the WORST Advice for Fat Loss and Health).

The ability for soluble fibers to feed our gut bacteria may sound healthy when it’s phrased as “feeding our good bacteria,” but this is more like wishful thinking. These fibers do feed our gut bacteria, but they feed the bad ones in addition to the good ones.

This isn’t a problem if our gut function and microbiome composition are optimal. But, if they aren’t optimal, which is extraordinarily common in modern times, this will exacerbate any gut dysfunction that’s going on.

(Fun fact: the gas that’s commonly associated with eating beans is a product of a suboptimal microbiome consuming soluble fiber)

On the other hand, the ability for insoluble fibers to move food through our gut is beneficial because gut motility is important for healthy gut function. But, this is a relatively trivial benefit in the context of grain consumption.

 

Grains, Legumes, and (Anti)nutrients

Whole grains, pseudograins, and legumes are touted for their nutrient content, specifically their vitamins, minerals, and protein. But when we consider their antinutrient content, their nutrient value is really pretty poor.

As I mentioned earlier, grains, pseudograins, and legumes are seeds. Seeds are an extraordinarily important part of plants – they’re needed for plants to reproduce. The nutrients in seeds aren’t meant for us, they’re meant to be used for growing a new plant.

Plants can’t protect their valuable seeds by running from predators or attacking them with sharp claws or teeth. Instead, their seeds have chemical defenses – compounds that protect their nutrients and cause harm to animals who eat them. These compounds are commonly referred to as antinutrients.

There are several types of antinutrients, including lectins, phytic acid (phytates), oxalic acid (oxalates), enzyme inhibitors, and saponins, each with unique harmful effects.

Lectins

Lectins are probably the most damaging and well-known antinutrients. You’ve probably heard of the most infamous lectin, gluten. Lectins inhibit nutrient absorption, cause bacterial overgrowth and systemic stress and inflammation, and damage our gut barrier, causing it to become permeable or “leaky” (2, 3, 4, 5, 6).

Gut permeability, or “leakiness,” allows undigested food particles and toxins to travel directly into the bloodstream, which can impair energy production and contribute to stress and inflammation (7, 8).

Phytic Acid and Oxalic Acid

Phytic acid and oxalic acid bind with calcium, magnesium, zinc, copper, potassium, iron, and other minerals, blocking their digestion and absorption in our guts and inhibiting our ability to use them (9, 10, 11). These minerals are vital for many processes, one of the most noteworthy being energy production.

Enzyme Inhibitors

Enzyme inhibitors block the enzymes in our guts that digest protein and starch, which prevents the digestion and absorption of protein and starches in the grains, pseudograins, and legumes, as well as in other foods we happen to be eating with them (9, 12, 13). Phytic acid also blocks some of these enzymes, further inhibiting the digestion of protein and starch (14, 15).

Saponins

Saponins, which are found mostly in pseudograins and legumes, inhibit protein-digesting enzymes, inhibit thyroid function (the regulator of our metabolism), and bind with and lower cholesterol (this isn’t beneficial, as we might be led to believe – I explain why here) (16, 17, 18).

 

Antinutrients No More

Somehow, the mainstream has found ways to spin the harmful effects of antinutrients into benefits. Impairing energy production and contributing to inflammation is considered “boosting immune function,” impairing starch digestion is considered “managing blood sugar,” and reducing cholesterol is, well, just reducing cholesterol, but this isn’t beneficial like we’ve been told.

If you ask me, it’s pretty clear that whole grains and legumes aren’t the health foods they’ve been made out to be. If anything, they appear to be worse than their obesity-, diabetes-, and heart disease-causing counterparts, refined grains. And this isn’t to mention the pesticides and GMOs that are ubiquitous among these crops.

But, it’s not all bad. In fact, grains and legumes can be prepared in ways that negate many of their negative effects. Cooking can deactivate a few of the antinutrients in these foods, but the traditional preparations of soaking, sprouting, and fermenting significantly reduce their antinutrient content, and may even alter their fiber composition (9, 19).

But if that doesn’t suit your fancy, you can skip these foods altogether!

Grains are most certainly not a necessary part of a healthy diet like they’ve been made out to be. Fruits and starch-containing foods that aren’t grains, including roots (carrots, yuca, turnips, etc.), tubers (potatoes and sweet potatoes), and vegetables in the gourd family (like squash and zucchini), are all great sources of carbohydrates with few antinutrients, if any.

(Note: some of these foods, like potatoes, do have antinutrients. But, they’re housed in the skins which can be easily removed.)

Also, while it is a grain, white rice is a relatively antinutrient-free carbohydrate source. This is because it’s stripped of its bran and hull, the parts of brown rice that contain most of the antinutrients.

Does all of this mean that if you eat any non-traditionally prepared grains, pseudograins, or legumes you can say goodbye to your health?

Of course not. But it does mean that their promotion as “health foods” is not supported, and we may want to reconsider how much of them we’re eating.

 

References

Grains and Legumes and Antinutrients, Oh My!

Despite the growing anti-grain movement, it’s still recommended that we consume 5-8 ounce equivalents or more of grains per day, and whole grains are still the face of the typical healthy diet (1).

Mainstream nutrition recommendations tell us that whole grains, pseudograins, and legumes are heart-healthy and promote a healthy weight. These food groups include foods like:

  • Wheat, corn, rye, barely, rice, millet, oats (grains)
  • Quinoa, amaranth, buckwheat (pseudograins)
  • Beans, soy, lentils, peanuts (legumes)

On the other hand, refined grains are the ones blamed for obesity, diabetes, and heart disease.

 

Holy Whole Grains vs. Evil Refined Grains

Let’s start with the basics.

Grains, pseudograins, and legumes are all seeds, which have 3 main components: bran, germ, and endosperm. The bran and germ contain most of the fiber and “nutrients,” and the endosperm is the carbohydrate-dense portion.

A whole grain is still intact – it contains all 3 of these components, while refined grains are stripped of the germ and bran, leaving only the endosperm.

So, the only difference between the “healthiest-of-all-foods” whole grains and the “inflammation-diabetes-obesity-and-heart-disease-causing” refined grains are the fiber and the “nutrients,” while the starch-containing endosperm is the same.

And, like whole grains, the “heart-healthy” pseudograins and legumes are full of fiber and “nutrients.”

But, it turns out that the fibers and “nutrients” found in these foods might not be so beneficial after all, leaving their supposed health-promoting effects in question.

 

Grains, Legumes, and Fiber

Whole grains, pseudograins, and legumes contain both soluble and insoluble fibers.

Soluble fibers are considered prebiotics because they feed our gut bacteria, whereas insoluble fibers are not digested by our gut bacteria and help to move food through our guts.

These fibers are considered beneficial because of ability to keep us full for longer, their prebiotic effects, and their colon cleansing effects.

But, these effects aren’t always so beneficial.

Keeping us full for longer might be favorable if we wanted to eat less, but eating less isn’t really beneficial unless we want to deprive ourselves of energy (Why “Eat Less and Exercise More” is the WORST Advice for Fat Loss and Health).

The ability for soluble fibers to feed our gut bacteria may sound healthy when it’s phrased as “feeding our good bacteria,” but this is more like wishful thinking. These fibers do feed our gut bacteria, but they feed the bad ones in addition to the good ones.

This isn’t a problem if our gut function and microbiome composition are optimal. But, if they aren’t optimal, which is extraordinarily common in modern times, this will exacerbate any gut dysfunction that’s going on.

(Fun fact: the gas that’s commonly associated with eating beans is a product of a suboptimal microbiome consuming soluble fiber)

On the other hand, the ability for insoluble fibers to move food through our gut is beneficial because gut motility is important for healthy gut function. But, this is a relatively trivial benefit in the context of grain consumption.

 

Grains, Legumes, and (Anti)nutrients

Whole grains, pseudograins, and legumes are touted for their nutrient content, specifically their vitamins, minerals, and protein. But when we consider their antinutrient content, their nutrient value is really pretty poor.

As I mentioned earlier, grains, pseudograins, and legumes are seeds. Seeds are an extraordinarily important part of plants – they’re needed for plants to reproduce. The nutrients in seeds aren’t meant for us, they’re meant to be used for growing a new plant.

Plants can’t protect their valuable seeds by running from predators or attacking them with sharp claws or teeth. Instead, their seeds have chemical defenses – compounds that protect their nutrients and cause harm to animals who eat them. These compounds are commonly referred to as antinutrients.

There are several types of antinutrients, including lectins, phytic acid (phytates), oxalic acid (oxalates), enzyme inhibitors, and saponins, each with unique harmful effects.

Lectins

Lectins are probably the most damaging and well-known antinutrients. You’ve probably heard of the most infamous lectin, gluten. Lectins inhibit nutrient absorption, cause bacterial overgrowth and systemic stress and inflammation, and damage our gut barrier, causing it to become permeable or “leaky” (2, 3, 4, 5, 6).

Gut permeability, or “leakiness,” allows undigested food particles and toxins to travel directly into the bloodstream, which can impair energy production and contribute to stress and inflammation (7, 8).

Phytic Acid and Oxalic Acid

Phytic acid and oxalic acid bind with calcium, magnesium, zinc, copper, potassium, iron, and other minerals, blocking their digestion and absorption in our guts and inhibiting our ability to use them (9, 10, 11). These minerals are vital for many processes, one of the most noteworthy being energy production.

Enzyme Inhibitors

Enzyme inhibitors block the enzymes in our guts that digest protein and starch, which prevents the digestion and absorption of protein and starches in the grains, pseudograins, and legumes, as well as in other foods we happen to be eating with them (9, 12, 13). Phytic acid also blocks some of these enzymes, further inhibiting the digestion of protein and starch (14, 15).

Saponins

Saponins, which are found mostly in pseudograins and legumes, inhibit protein-digesting enzymes, inhibit thyroid function (the regulator of our metabolism), and bind with and lower cholesterol (this isn’t beneficial, as we might be led to believe – I explain why here) (16, 17, 18).

 

Antinutrients No More

Somehow, the mainstream has found ways to spin the harmful effects of antinutrients into benefits. Impairing energy production and contributing to inflammation is considered “boosting immune function,” impairing starch digestion is considered “managing blood sugar,” and reducing cholesterol is, well, just reducing cholesterol, but this isn’t beneficial like we’ve been told.

If you ask me, it’s pretty clear that whole grains and legumes aren’t the health foods they’ve been made out to be. If anything, they appear to be worse than their obesity-, diabetes-, and heart disease-causing counterparts, refined grains. And this isn’t to mention the pesticides and GMOs that are ubiquitous among these crops.

But, it’s not all bad. In fact, grains and legumes can be prepared in ways that negate many of their negative effects. Cooking can deactivate a few of the antinutrients in these foods, but the traditional preparations of soaking, sprouting, and fermenting significantly reduce their antinutrient content, and may even alter their fiber composition (9, 19).

But if that doesn’t suit your fancy, you can skip these foods altogether!

Grains are most certainly not a necessary part of a healthy diet like they’ve been made out to be. Fruits and starch-containing foods that aren’t grains, including roots (carrots, yuca, turnips, etc.), tubers (potatoes and sweet potatoes), and vegetables in the gourd family (like squash and zucchini), are all great sources of carbohydrates with few antinutrients, if any.

(Note: some of these foods, like potatoes, do have antinutrients. But, they’re housed in the skins which can be easily removed.)

Also, while it is a grain, white rice is a relatively antinutrient-free carbohydrate source. This is because it’s stripped of its bran and hull, the parts of brown rice that contain most of the antinutrients.

Does all of this mean that if you eat any non-traditionally prepared grains, pseudograins, or legumes you can say goodbye to your health?

Of course not. But it does mean that their promotion as “health foods” is not supported, and we may want to reconsider how much of them we’re eating.

 

References

Grains and Legumes and Antinutrients, Oh My!

Despite the growing anti-grain movement, it’s still recommended that we consume 5-8 ounce equivalents or more of grains per day, and whole grains are still the face of the typical healthy diet (1).

Mainstream nutrition recommendations tell us that whole grains, pseudograins, and legumes are heart-healthy and promote a healthy weight. These food groups include foods like:

  • Wheat, corn, rye, barely, rice, millet, oats (grains)
  • Quinoa, amaranth, buckwheat (pseudograins)
  • Beans, soy, lentils, peanuts (legumes)

On the other hand, refined grains are the ones blamed for obesity, diabetes, and heart disease.

 

Holy Whole Grains vs. Evil Refined Grains

Let’s start with the basics.

Grains, pseudograins, and legumes are all seeds, which have 3 main components: bran, germ, and endosperm. The bran and germ contain most of the fiber and “nutrients,” and the endosperm is the carbohydrate-dense portion.

A whole grain is still intact – it contains all 3 of these components, while refined grains are stripped of the germ and bran, leaving only the endosperm.

So, the only difference between the “healthiest-of-all-foods” whole grains and the “inflammation-diabetes-obesity-and-heart-disease-causing” refined grains are the fiber and the “nutrients,” while the starch-containing endosperm is the same.

And, like whole grains, the “heart-healthy” pseudograins and legumes are full of fiber and “nutrients.”

But, it turns out that the fibers and “nutrients” found in these foods might not be so beneficial after all, leaving their supposed health-promoting effects in question.

 

Grains, Legumes, and Fiber

Whole grains, pseudograins, and legumes contain both soluble and insoluble fibers.

Soluble fibers are considered prebiotics because they feed our gut bacteria, whereas insoluble fibers are not digested by our gut bacteria and help to move food through our guts.

These fibers are considered beneficial because of ability to keep us full for longer, their prebiotic effects, and their colon cleansing effects.

But, these effects aren’t always so beneficial.

Keeping us full for longer might be favorable if we wanted to eat less, but eating less isn’t really beneficial unless we want to deprive ourselves of energy (Why “Eat Less and Exercise More” is the WORST Advice for Fat Loss and Health).

The ability for soluble fibers to feed our gut bacteria may sound healthy when it’s phrased as “feeding our good bacteria,” but this is more like wishful thinking. These fibers do feed our gut bacteria, but they feed the bad ones in addition to the good ones.

This isn’t a problem if our gut function and microbiome composition are optimal. But, if they aren’t optimal, which is extraordinarily common in modern times, this will exacerbate any gut dysfunction that’s going on.

(Fun fact: the gas that’s commonly associated with eating beans is a product of a suboptimal microbiome consuming soluble fiber)

On the other hand, the ability for insoluble fibers to move food through our gut is beneficial because gut motility is important for healthy gut function. But, this is a relatively trivial benefit in the context of grain consumption.

 

Grains, Legumes, and (Anti)nutrients

Whole grains, pseudograins, and legumes are touted for their nutrient content, specifically their vitamins, minerals, and protein. But when we consider their antinutrient content, their nutrient value is really pretty poor.

As I mentioned earlier, grains, pseudograins, and legumes are seeds. Seeds are an extraordinarily important part of plants – they’re needed for plants to reproduce. The nutrients in seeds aren’t meant for us, they’re meant to be used for growing a new plant.

Plants can’t protect their valuable seeds by running from predators or attacking them with sharp claws or teeth. Instead, their seeds have chemical defenses – compounds that protect their nutrients and cause harm to animals who eat them. These compounds are commonly referred to as antinutrients.

There are several types of antinutrients, including lectins, phytic acid (phytates), oxalic acid (oxalates), enzyme inhibitors, and saponins, each with unique harmful effects.

Lectins

Lectins are probably the most damaging and well-known antinutrients. You’ve probably heard of the most infamous lectin, gluten. Lectins inhibit nutrient absorption, cause bacterial overgrowth and systemic stress and inflammation, and damage our gut barrier, causing it to become permeable or “leaky” (2, 3, 4, 5, 6).

Gut permeability, or “leakiness,” allows undigested food particles and toxins to travel directly into the bloodstream, which can impair energy production and contribute to stress and inflammation (7, 8).

Phytic Acid and Oxalic Acid

Phytic acid and oxalic acid bind with calcium, magnesium, zinc, copper, potassium, iron, and other minerals, blocking their digestion and absorption in our guts and inhibiting our ability to use them (9, 10, 11). These minerals are vital for many processes, one of the most noteworthy being energy production.

Enzyme Inhibitors

Enzyme inhibitors block the enzymes in our guts that digest protein and starch, which prevents the digestion and absorption of protein and starches in the grains, pseudograins, and legumes, as well as in other foods we happen to be eating with them (9, 12, 13). Phytic acid also blocks some of these enzymes, further inhibiting the digestion of protein and starch (14, 15).

Saponins

Saponins, which are found mostly in pseudograins and legumes, inhibit protein-digesting enzymes, inhibit thyroid function (the regulator of our metabolism), and bind with and lower cholesterol (this isn’t beneficial, as we might be led to believe – I explain why here) (16, 17, 18).

 

Antinutrients No More

Somehow, the mainstream has found ways to spin the harmful effects of antinutrients into benefits. Impairing energy production and contributing to inflammation is considered “boosting immune function,” impairing starch digestion is considered “managing blood sugar,” and reducing cholesterol is, well, just reducing cholesterol, but this isn’t beneficial like we’ve been told.

If you ask me, it’s pretty clear that whole grains and legumes aren’t the health foods they’ve been made out to be. If anything, they appear to be worse than their obesity-, diabetes-, and heart disease-causing counterparts, refined grains. And this isn’t to mention the pesticides and GMOs that are ubiquitous among these crops.

But, it’s not all bad. In fact, grains and legumes can be prepared in ways that negate many of their negative effects. Cooking can deactivate a few of the antinutrients in these foods, but the traditional preparations of soaking, sprouting, and fermenting significantly reduce their antinutrient content, and may even alter their fiber composition (9, 19).

But if that doesn’t suit your fancy, you can skip these foods altogether!

Grains are most certainly not a necessary part of a healthy diet like they’ve been made out to be. Fruits and starch-containing foods that aren’t grains, including roots (carrots, yuca, turnips, etc.), tubers (potatoes and sweet potatoes), and vegetables in the gourd family (like squash and zucchini), are all great sources of carbohydrates with few antinutrients, if any.

(Note: some of these foods, like potatoes, do have antinutrients. But, they’re housed in the skins which can be easily removed.)

Also, while it is a grain, white rice is a relatively antinutrient-free carbohydrate source. This is because it’s stripped of its bran and hull, the parts of brown rice that contain most of the antinutrients.

Does all of this mean that if you eat any non-traditionally prepared grains, pseudograins, or legumes you can say goodbye to your health?

Of course not. But it does mean that their promotion as “health foods” is not supported, and we may want to reconsider how much of them we’re eating.

 

References

Are You Still Restricting Salt?

I was planning on writing about the current salt and sodium recommendations and the lack of solid research supporting them, but I realized that there are already enough comprehensive articles written about that (like this one). Instead, I’ll quickly summarize the absurdity of the current sodium recommendations and focus on the problems caused by restricting salt.

 

Some Ridiculous Guidelines

The current Dietary Guidelines for Americans recommend that we consume less than 2,300 mg sodium per day and less than 1,500 mg sodium for individuals with high blood pressure (1), the World Health Organization recommends that we consume less than 2,000 mg sodium per day (2), and the American Heart Association recommends an ideal limit of no more than 1,500 mg sodium per day for most adults (3).

These recommendations are aimed at reducing hypertension and cardiovascular disease. However, they’re at odds with much of the research, which shows that the current sodium recommendations are between 2 and 4 times lower than what is ideal for cardiovascular health and health in general.

Sodium intakes of 4,000-6,000 mg per day are associated with the lowest risk of cardiovascular death and hospitalization for congestive heart failure (4) while consuming under 2,300 mg sodium per day is associated with increased cardiovascular disease mortality and all-cause mortality (5). And, even consuming less than 3,600 mg per day is associated with greater cardiovascular disease mortality (6).

 

Sodium, the (Almost) Perfect Scapegoat

Ridiculous recommendations aside, sodium is an extraordinarily important mineral that has been wrongly blamed for causing hypertension and cardiovascular disease. This blame comes primarily from sodium’s ability to attract water.

When we consume sodium, the amount of sodium in our blood increases, which increases our blood volume because sodium attracts water.

Our blood pressure is a function of the volume of blood in circulation and the constriction or relaxation of our blood vessels. When our blood volume increases or blood vessels constrict, our blood pressure increases, and vice versa.

So, it’s assumed that increasing sodium consumption increases blood pressure by increasing the blood volume. It’s then assumed that this high blood pressure leads to cardiovascular disease. By the same line of thinking, sodium is blamed for increasing swelling, bloating, and water retention due to its attraction for water.

But, like the “calories-in versus calories-out” model of fat loss, these ideas are based on oversimplified models of the human body that ignore that we adapt to our environments.

When the blood volume is increased from increased salt consumption, our bodies adapt by increasing the amount of sodium they excrete and relaxing our blood vessels. This allows us to maintain a relatively steady blood pressure, while also allowing for optimal blood flow, mineral balance, and energy production. This is easier to explain by describing what happens when we don’t consume enough sodium.

 

What Happens When We Don’t Consume Enough Salt?

Contrary to the mainstream ideas, a low salt intake actually contributes to poor cardiovascular health and swelling and bloating.

When we reduce our salt intake, the amount of sodium in the blood is reduced, which causes an immediate reduction in blood volume and blood pressure. This is why reducing salt intake is suggested for reducing high blood pressure.

But it doesn’t end there.

Maintaining adequate blood pressure is extremely important for transporting nutrients and waste throughout our bodies. So, when our blood pressure is acutely reduced, our stress systems are activated in response (7).

Our stress systems constrict our blood vessels and release the stress hormone aldosterone, which reduces the amount of sodium that we excrete in our kidneys, allowing us to maintain higher sodium (and water) levels in our blood (8). This keeps our blood volume and blood pressure at the levels needed to transport nutrients and waste throughout the body.

But, while this balancing act allows us to maintain blood volume and blood pressure in the short term, it comes at a cost: the sodium we would normally excrete in our kidneys is replaced with potassium and magnesium (9). This means that when we reduce our salt consumption, we lose greater amounts of potassium and magnesium.

Like other adaptive processes, this isn’t a problem in acute situations. But when continued chronically, losing potassium and magnesium can contribute to high blood pressure and inhibit our bodies’ ability to produce energy.

 

Sodium, Swelling, and Energy Production

Potassium and magnesium are balanced with sodium in the cellular environment. Potassium and magnesium are housed within our cells, while sodium remains outside of the cell. This also keeps water outside of the cells (with sodium), which is an important feature of a healthy cell.

When we lose potassium and magnesium due to a low sodium intake, there is less potassium and magnesium in our cells. This then allows more sodium to enter the cell, bringing water with it, which causes the cell to swell (10). The increase in aldosterone due to a low sodium intake also contributes to this cell swelling (11, 12, 13).

This swelling is a real problem – a swollen cell can’t properly produce or use energy (14). Not only is this disastrous for our metabolism, which lies at the foundation of our health, but it can also contribute to cardiovascular problems!

When the cells in our blood vessels swell due to their lack of potassium and magnesium, it inhibits their ability to relax and causes our blood vessels to constrict (like a swollen muscle after working out) (15, 16, 17). This helps to make up for the reduced blood volume from less salt consumption, but also restricts blood flow throughout our bodies and can cause other cardiovascular problems.

In other words, when we eat less salt, our blood pressure is maintained via our stress systems. But, when this occurs over time, we lose potassium and magnesium, leading to cell swelling that inhibits energy production and can cause cardiovascular problems.

 

How Much Salt Should We Eat?

Eating too little salt increases stress, reduces the metabolism, and can lead to cardiovascular problems in the long-term (7, 18, 19).

On the other hand, consuming enough salt allows for optimal energy production, adequate blood volume, reduced swelling and bloating, and sparing of potassium and magnesium. This allows for proper metabolic function, cardiovascular function, and really all other functions.

So, should we eat salt to our heart’s content?

Pretty much! Our sense of taste has been designed to dictate our nutrient intake. When we don’t have enough sodium, we have a stronger desire to eat salty foods, and vice versa (20). So, we can just listen to what our bodies need and allow that to dictate how much salt we consume.

In other words, salt to taste!

If you’re worried about your blood pressure, then make sure you’re getting enough potassium and magnesium. Reducing sodium intake may drop your blood pressure a few points, but it doesn’t translate to better cardiovascular health.

 

References

Are You Still Restricting Salt?

I was planning on writing about the current salt and sodium recommendations and the lack of solid research supporting them, but I realized that there are already enough comprehensive articles written about that (like this one). Instead, I’ll quickly summarize the absurdity of the current sodium recommendations and focus on the problems caused by restricting salt.

 

Some Ridiculous Guidelines

The current Dietary Guidelines for Americans recommend that we consume less than 2,300 mg sodium per day and less than 1,500 mg sodium for individuals with high blood pressure (1), the World Health Organization recommends that we consume less than 2,000 mg sodium per day (2), and the American Heart Association recommends an ideal limit of no more than 1,500 mg sodium per day for most adults (3).

These recommendations are aimed at reducing hypertension and cardiovascular disease. However, they’re at odds with much of the research, which shows that the current sodium recommendations are between 2 and 4 times lower than what is ideal for cardiovascular health and health in general.

Sodium intakes of 4,000-6,000 mg per day are associated with the lowest risk of cardiovascular death and hospitalization for congestive heart failure (4) while consuming under 2,300 mg sodium per day is associated with increased cardiovascular disease mortality and all-cause mortality (5). And, even consuming less than 3,600 mg per day is associated with greater cardiovascular disease mortality (6).

 

Sodium, the (Almost) Perfect Scapegoat

Ridiculous recommendations aside, sodium is an extraordinarily important mineral that has been wrongly blamed for causing hypertension and cardiovascular disease. This blame comes primarily from sodium’s ability to attract water.

When we consume sodium, the amount of sodium in our blood increases, which increases our blood volume because sodium attracts water.

Our blood pressure is a function of the volume of blood in circulation and the constriction or relaxation of our blood vessels. When our blood volume increases or blood vessels constrict, our blood pressure increases, and vice versa.

So, it’s assumed that increasing sodium consumption increases blood pressure by increasing the blood volume. It’s then assumed that this high blood pressure leads to cardiovascular disease. By the same line of thinking, sodium is blamed for increasing swelling, bloating, and water retention due to its attraction for water.

But, like the “calories-in versus calories-out” model of fat loss, these ideas are based on oversimplified models of the human body that ignore that we adapt to our environments.

When the blood volume is increased from increased salt consumption, our bodies adapt by increasing the amount of sodium they excrete and relaxing our blood vessels. This allows us to maintain a relatively steady blood pressure, while also allowing for optimal blood flow, mineral balance, and energy production. This is easier to explain by describing what happens when we don’t consume enough sodium.

 

What Happens When We Don’t Consume Enough Salt?

Contrary to the mainstream ideas, a low salt intake actually contributes to poor cardiovascular health and swelling and bloating.

When we reduce our salt intake, the amount of sodium in the blood is reduced, which causes an immediate reduction in blood volume and blood pressure. This is why reducing salt intake is suggested for reducing high blood pressure.

But it doesn’t end there.

Maintaining adequate blood pressure is extremely important for transporting nutrients and waste throughout our bodies. So, when our blood pressure is acutely reduced, our stress systems are activated in response (7).

Our stress systems constrict our blood vessels and release the stress hormone aldosterone, which reduces the amount of sodium that we excrete in our kidneys, allowing us to maintain higher sodium (and water) levels in our blood (8). This keeps our blood volume and blood pressure at the levels needed to transport nutrients and waste throughout the body.

But, while this balancing act allows us to maintain blood volume and blood pressure in the short term, it comes at a cost: the sodium we would normally excrete in our kidneys is replaced with potassium and magnesium (9). This means that when we reduce our salt consumption, we lose greater amounts of potassium and magnesium.

Like other adaptive processes, this isn’t a problem in acute situations. But when continued chronically, losing potassium and magnesium can contribute to high blood pressure and inhibit our bodies’ ability to produce energy.

 

Sodium, Swelling, and Energy Production

Potassium and magnesium are balanced with sodium in the cellular environment. Potassium and magnesium are housed within our cells, while sodium remains outside of the cell. This also keeps water outside of the cells (with sodium), which is an important feature of a healthy cell.

When we lose potassium and magnesium due to a low sodium intake, there is less potassium and magnesium in our cells. This then allows more sodium to enter the cell, bringing water with it, which causes the cell to swell (10). The increase in aldosterone due to a low sodium intake also contributes to this cell swelling (11, 12, 13).

This swelling is a real problem – a swollen cell can’t properly produce or use energy (14). Not only is this disastrous for our metabolism, which lies at the foundation of our health, but it can also contribute to cardiovascular problems!

When the cells in our blood vessels swell due to their lack of potassium and magnesium, it inhibits their ability to relax and causes our blood vessels to constrict (like a swollen muscle after working out) (15, 16, 17). This helps to make up for the reduced blood volume from less salt consumption, but also restricts blood flow throughout our bodies and can cause other cardiovascular problems.

In other words, when we eat less salt, our blood pressure is maintained via our stress systems. But, when this occurs over time, we lose potassium and magnesium, leading to cell swelling that inhibits energy production and can cause cardiovascular problems.

 

How Much Salt Should We Eat?

Eating too little salt increases stress, reduces the metabolism, and can lead to cardiovascular problems in the long-term (7, 18, 19).

On the other hand, consuming enough salt allows for optimal energy production, adequate blood volume, reduced swelling and bloating, and sparing of potassium and magnesium. This allows for proper metabolic function, cardiovascular function, and really all other functions.

So, should we eat salt to our heart’s content?

Pretty much! Our sense of taste has been designed to dictate our nutrient intake. When we don’t have enough sodium, we have a stronger desire to eat salty foods, and vice versa (20). So, we can just listen to what our bodies need and allow that to dictate how much salt we consume.

In other words, salt to taste!

If you’re worried about your blood pressure, then make sure you’re getting enough potassium and magnesium. Reducing sodium intake may drop your blood pressure a few points, but it doesn’t translate to better cardiovascular health.

 

References

Are You Still Restricting Salt?

I was planning on writing about the current salt and sodium recommendations and the lack of solid research supporting them, but I realized that there are already enough comprehensive articles written about that (like this one). Instead, I’ll quickly summarize the absurdity of the current sodium recommendations and focus on the problems caused by restricting salt.

 

Some Ridiculous Guidelines

The current Dietary Guidelines for Americans recommend that we consume less than 2,300 mg sodium per day and less than 1,500 mg sodium for individuals with high blood pressure (1), the World Health Organization recommends that we consume less than 2,000 mg sodium per day (2), and the American Heart Association recommends an ideal limit of no more than 1,500 mg sodium per day for most adults (3).

These recommendations are aimed at reducing hypertension and cardiovascular disease. However, they’re at odds with much of the research, which shows that the current sodium recommendations are between 2 and 4 times lower than what is ideal for cardiovascular health and health in general.

Sodium intakes of 4,000-6,000 mg per day are associated with the lowest risk of cardiovascular death and hospitalization for congestive heart failure (4) while consuming under 2,300 mg sodium per day is associated with increased cardiovascular disease mortality and all-cause mortality (5). And, even consuming less than 3,600 mg per day is associated with greater cardiovascular disease mortality (6).

 

Sodium, the (Almost) Perfect Scapegoat

Ridiculous recommendations aside, sodium is an extraordinarily important mineral that has been wrongly blamed for causing hypertension and cardiovascular disease. This blame comes primarily from sodium’s ability to attract water.

When we consume sodium, the amount of sodium in our blood increases, which increases our blood volume because sodium attracts water.

Our blood pressure is a function of the volume of blood in circulation and the constriction or relaxation of our blood vessels. When our blood volume increases or blood vessels constrict, our blood pressure increases, and vice versa.

So, it’s assumed that increasing sodium consumption increases blood pressure by increasing the blood volume. It’s then assumed that this high blood pressure leads to cardiovascular disease. By the same line of thinking, sodium is blamed for increasing swelling, bloating, and water retention due to its attraction for water.

But, like the “calories-in versus calories-out” model of fat loss, these ideas are based on oversimplified models of the human body that ignore that we adapt to our environments.

When the blood volume is increased from increased salt consumption, our bodies adapt by increasing the amount of sodium they excrete and relaxing our blood vessels. This allows us to maintain a relatively steady blood pressure, while also allowing for optimal blood flow, mineral balance, and energy production. This is easier to explain by describing what happens when we don’t consume enough sodium.

 

What Happens When We Don’t Consume Enough Salt?

Contrary to the mainstream ideas, a low salt intake actually contributes to poor cardiovascular health and swelling and bloating.

When we reduce our salt intake, the amount of sodium in the blood is reduced, which causes an immediate reduction in blood volume and blood pressure. This is why reducing salt intake is suggested for reducing high blood pressure.

But it doesn’t end there.

Maintaining adequate blood pressure is extremely important for transporting nutrients and waste throughout our bodies. So, when our blood pressure is acutely reduced, our stress systems are activated in response (7).

Our stress systems constrict our blood vessels and release the stress hormone aldosterone, which reduces the amount of sodium that we excrete in our kidneys, allowing us to maintain higher sodium (and water) levels in our blood (8). This keeps our blood volume and blood pressure at the levels needed to transport nutrients and waste throughout the body.

But, while this balancing act allows us to maintain blood volume and blood pressure in the short term, it comes at a cost: the sodium we would normally excrete in our kidneys is replaced with potassium and magnesium (9). This means that when we reduce our salt consumption, we lose greater amounts of potassium and magnesium.

Like other adaptive processes, this isn’t a problem in acute situations. But when continued chronically, losing potassium and magnesium can contribute to high blood pressure and inhibit our bodies’ ability to produce energy.

 

Sodium, Swelling, and Energy Production

Potassium and magnesium are balanced with sodium in the cellular environment. Potassium and magnesium are housed within our cells, while sodium remains outside of the cell. This also keeps water outside of the cells (with sodium), which is an important feature of a healthy cell.

When we lose potassium and magnesium due to a low sodium intake, there is less potassium and magnesium in our cells. This then allows more sodium to enter the cell, bringing water with it, which causes the cell to swell (10). The increase in aldosterone due to a low sodium intake also contributes to this cell swelling (11, 12, 13).

This swelling is a real problem – a swollen cell can’t properly produce or use energy (14). Not only is this disastrous for our metabolism, which lies at the foundation of our health, but it can also contribute to cardiovascular problems!

When the cells in our blood vessels swell due to their lack of potassium and magnesium, it inhibits their ability to relax and causes our blood vessels to constrict (like a swollen muscle after working out) (15, 16, 17). This helps to make up for the reduced blood volume from less salt consumption, but also restricts blood flow throughout our bodies and can cause other cardiovascular problems.

In other words, when we eat less salt, our blood pressure is maintained via our stress systems. But, when this occurs over time, we lose potassium and magnesium, leading to cell swelling that inhibits energy production and can cause cardiovascular problems.

 

How Much Salt Should We Eat?

Eating too little salt increases stress, reduces the metabolism, and can lead to cardiovascular problems in the long-term (7, 18, 19).

On the other hand, consuming enough salt allows for optimal energy production, adequate blood volume, reduced swelling and bloating, and sparing of potassium and magnesium. This allows for proper metabolic function, cardiovascular function, and really all other functions.

So, should we eat salt to our heart’s content?

Pretty much! Our sense of taste has been designed to dictate our nutrient intake. When we don’t have enough sodium, we have a stronger desire to eat salty foods, and vice versa (20). So, we can just listen to what our bodies need and allow that to dictate how much salt we consume.

In other words, salt to taste!

If you’re worried about your blood pressure, then make sure you’re getting enough potassium and magnesium. Reducing sodium intake may drop your blood pressure a few points, but it doesn’t translate to better cardiovascular health.

 

References

Are You Still Restricting Salt?

I was planning on writing about the current salt and sodium recommendations and the lack of solid research supporting them, but I realized that there are already enough comprehensive articles written about that (like this one). Instead, I’ll quickly summarize the absurdity of the current sodium recommendations and focus on the problems caused by restricting salt.

 

Some Ridiculous Guidelines

The current Dietary Guidelines for Americans recommend that we consume less than 2,300 mg sodium per day and less than 1,500 mg sodium for individuals with high blood pressure (1), the World Health Organization recommends that we consume less than 2,000 mg sodium per day (2), and the American Heart Association recommends an ideal limit of no more than 1,500 mg sodium per day for most adults (3).

These recommendations are aimed at reducing hypertension and cardiovascular disease. However, they’re at odds with much of the research, which shows that the current sodium recommendations are between 2 and 4 times lower than what is ideal for cardiovascular health and health in general.

Sodium intakes of 4,000-6,000 mg per day are associated with the lowest risk of cardiovascular death and hospitalization for congestive heart failure (4) while consuming under 2,300 mg sodium per day is associated with increased cardiovascular disease mortality and all-cause mortality (5). And, even consuming less than 3,600 mg per day is associated with greater cardiovascular disease mortality (6).

 

Sodium, the (Almost) Perfect Scapegoat

Ridiculous recommendations aside, sodium is an extraordinarily important mineral that has been wrongly blamed for causing hypertension and cardiovascular disease. This blame comes primarily from sodium’s ability to attract water.

When we consume sodium, the amount of sodium in our blood increases, which increases our blood volume because sodium attracts water.

Our blood pressure is a function of the volume of blood in circulation and the constriction or relaxation of our blood vessels. When our blood volume increases or blood vessels constrict, our blood pressure increases, and vice versa.

So, it’s assumed that increasing sodium consumption increases blood pressure by increasing the blood volume. It’s then assumed that this high blood pressure leads to cardiovascular disease. By the same line of thinking, sodium is blamed for increasing swelling, bloating, and water retention due to its attraction for water.

But, like the “calories-in versus calories-out” model of fat loss, these ideas are based on oversimplified models of the human body that ignore that we adapt to our environments.

When the blood volume is increased from increased salt consumption, our bodies adapt by increasing the amount of sodium they excrete and relaxing our blood vessels. This allows us to maintain a relatively steady blood pressure, while also allowing for optimal blood flow, mineral balance, and energy production. This is easier to explain by describing what happens when we don’t consume enough sodium.

 

What Happens When We Don’t Consume Enough Salt?

Contrary to the mainstream ideas, a low salt intake actually contributes to poor cardiovascular health and swelling and bloating.

When we reduce our salt intake, the amount of sodium in the blood is reduced, which causes an immediate reduction in blood volume and blood pressure. This is why reducing salt intake is suggested for reducing high blood pressure.

But it doesn’t end there.

Maintaining adequate blood pressure is extremely important for transporting nutrients and waste throughout our bodies. So, when our blood pressure is acutely reduced, our stress systems are activated in response (7).

Our stress systems constrict our blood vessels and release the stress hormone aldosterone, which reduces the amount of sodium that we excrete in our kidneys, allowing us to maintain higher sodium (and water) levels in our blood (8). This keeps our blood volume and blood pressure at the levels needed to transport nutrients and waste throughout the body.

But, while this balancing act allows us to maintain blood volume and blood pressure in the short term, it comes at a cost: the sodium we would normally excrete in our kidneys is replaced with potassium and magnesium (9). This means that when we reduce our salt consumption, we lose greater amounts of potassium and magnesium.

Like other adaptive processes, this isn’t a problem in acute situations. But when continued chronically, losing potassium and magnesium can contribute to high blood pressure and inhibit our bodies’ ability to produce energy.

 

Sodium, Swelling, and Energy Production

Potassium and magnesium are balanced with sodium in the cellular environment. Potassium and magnesium are housed within our cells, while sodium remains outside of the cell. This also keeps water outside of the cells (with sodium), which is an important feature of a healthy cell.

When we lose potassium and magnesium due to a low sodium intake, there is less potassium and magnesium in our cells. This then allows more sodium to enter the cell, bringing water with it, which causes the cell to swell (10). The increase in aldosterone due to a low sodium intake also contributes to this cell swelling (11, 12, 13).

This swelling is a real problem – a swollen cell can’t properly produce or use energy (14). Not only is this disastrous for our metabolism, which lies at the foundation of our health, but it can also contribute to cardiovascular problems!

When the cells in our blood vessels swell due to their lack of potassium and magnesium, it inhibits their ability to relax and causes our blood vessels to constrict (like a swollen muscle after working out) (15, 16, 17). This helps to make up for the reduced blood volume from less salt consumption, but also restricts blood flow throughout our bodies and can cause other cardiovascular problems.

In other words, when we eat less salt, our blood pressure is maintained via our stress systems. But, when this occurs over time, we lose potassium and magnesium, leading to cell swelling that inhibits energy production and can cause cardiovascular problems.

 

How Much Salt Should We Eat?

Eating too little salt increases stress, reduces the metabolism, and can lead to cardiovascular problems in the long-term (7, 18, 19).

On the other hand, consuming enough salt allows for optimal energy production, adequate blood volume, reduced swelling and bloating, and sparing of potassium and magnesium. This allows for proper metabolic function, cardiovascular function, and really all other functions.

So, should we eat salt to our heart’s content?

Pretty much! Our sense of taste has been designed to dictate our nutrient intake. When we don’t have enough sodium, we have a stronger desire to eat salty foods, and vice versa (20). So, we can just listen to what our bodies need and allow that to dictate how much salt we consume.

In other words, salt to taste!

If you’re worried about your blood pressure, then make sure you’re getting enough potassium and magnesium. Reducing sodium intake may drop your blood pressure a few points, but it doesn’t translate to better cardiovascular health.

 

References

Are You Still Restricting Salt?

I was planning on writing about the current salt and sodium recommendations and the lack of solid research supporting them, but I realized that there are already enough comprehensive articles written about that (like this one). Instead, I’ll quickly summarize the absurdity of the current sodium recommendations and focus on the problems caused by restricting salt.

 

Some Ridiculous Guidelines

The current Dietary Guidelines for Americans recommend that we consume less than 2,300 mg sodium per day and less than 1,500 mg sodium for individuals with high blood pressure (1), the World Health Organization recommends that we consume less than 2,000 mg sodium per day (2), and the American Heart Association recommends an ideal limit of no more than 1,500 mg sodium per day for most adults (3).

These recommendations are aimed at reducing hypertension and cardiovascular disease. However, they’re at odds with much of the research, which shows that the current sodium recommendations are between 2 and 4 times lower than what is ideal for cardiovascular health and health in general.

Sodium intakes of 4,000-6,000 mg per day are associated with the lowest risk of cardiovascular death and hospitalization for congestive heart failure (4) while consuming under 2,300 mg sodium per day is associated with increased cardiovascular disease mortality and all-cause mortality (5). And, even consuming less than 3,600 mg per day is associated with greater cardiovascular disease mortality (6).

 

Sodium, the (Almost) Perfect Scapegoat

Ridiculous recommendations aside, sodium is an extraordinarily important mineral that has been wrongly blamed for causing hypertension and cardiovascular disease. This blame comes primarily from sodium’s ability to attract water.

When we consume sodium, the amount of sodium in our blood increases, which increases our blood volume because sodium attracts water.

Our blood pressure is a function of the volume of blood in circulation and the constriction or relaxation of our blood vessels. When our blood volume increases or blood vessels constrict, our blood pressure increases, and vice versa.

So, it’s assumed that increasing sodium consumption increases blood pressure by increasing the blood volume. It’s then assumed that this high blood pressure leads to cardiovascular disease. By the same line of thinking, sodium is blamed for increasing swelling, bloating, and water retention due to its attraction for water.

But, like the “calories-in versus calories-out” model of fat loss, these ideas are based on oversimplified models of the human body that ignore that we adapt to our environments.

When the blood volume is increased from increased salt consumption, our bodies adapt by increasing the amount of sodium they excrete and relaxing our blood vessels. This allows us to maintain a relatively steady blood pressure, while also allowing for optimal blood flow, mineral balance, and energy production. This is easier to explain by describing what happens when we don’t consume enough sodium.

 

What Happens When We Don’t Consume Enough Salt?

Contrary to the mainstream ideas, a low salt intake actually contributes to poor cardiovascular health and swelling and bloating.

When we reduce our salt intake, the amount of sodium in the blood is reduced, which causes an immediate reduction in blood volume and blood pressure. This is why reducing salt intake is suggested for reducing high blood pressure.

But it doesn’t end there.

Maintaining adequate blood pressure is extremely important for transporting nutrients and waste throughout our bodies. So, when our blood pressure is acutely reduced, our stress systems are activated in response (7).

Our stress systems constrict our blood vessels and release the stress hormone aldosterone, which reduces the amount of sodium that we excrete in our kidneys, allowing us to maintain higher sodium (and water) levels in our blood (8). This keeps our blood volume and blood pressure at the levels needed to transport nutrients and waste throughout the body.

But, while this balancing act allows us to maintain blood volume and blood pressure in the short term, it comes at a cost: the sodium we would normally excrete in our kidneys is replaced with potassium and magnesium (9). This means that when we reduce our salt consumption, we lose greater amounts of potassium and magnesium.

Like other adaptive processes, this isn’t a problem in acute situations. But when continued chronically, losing potassium and magnesium can contribute to high blood pressure and inhibit our bodies’ ability to produce energy.

 

Sodium, Swelling, and Energy Production

Potassium and magnesium are balanced with sodium in the cellular environment. Potassium and magnesium are housed within our cells, while sodium remains outside of the cell. This also keeps water outside of the cells (with sodium), which is an important feature of a healthy cell.

When we lose potassium and magnesium due to a low sodium intake, there is less potassium and magnesium in our cells. This then allows more sodium to enter the cell, bringing water with it, which causes the cell to swell (10). The increase in aldosterone due to a low sodium intake also contributes to this cell swelling (11, 12, 13).

This swelling is a real problem – a swollen cell can’t properly produce or use energy (14). Not only is this disastrous for our metabolism, which lies at the foundation of our health, but it can also contribute to cardiovascular problems!

When the cells in our blood vessels swell due to their lack of potassium and magnesium, it inhibits their ability to relax and causes our blood vessels to constrict (like a swollen muscle after working out) (15, 16, 17). This helps to make up for the reduced blood volume from less salt consumption, but also restricts blood flow throughout our bodies and can cause other cardiovascular problems.

In other words, when we eat less salt, our blood pressure is maintained via our stress systems. But, when this occurs over time, we lose potassium and magnesium, leading to cell swelling that inhibits energy production and can cause cardiovascular problems.

 

How Much Salt Should We Eat?

Eating too little salt increases stress, reduces the metabolism, and can lead to cardiovascular problems in the long-term (7, 18, 19).

On the other hand, consuming enough salt allows for optimal energy production, adequate blood volume, reduced swelling and bloating, and sparing of potassium and magnesium. This allows for proper metabolic function, cardiovascular function, and really all other functions.

So, should we eat salt to our heart’s content?

Pretty much! Our sense of taste has been designed to dictate our nutrient intake. When we don’t have enough sodium, we have a stronger desire to eat salty foods, and vice versa (20). So, we can just listen to what our bodies need and allow that to dictate how much salt we consume.

In other words, salt to taste!

If you’re worried about your blood pressure, then make sure you’re getting enough potassium and magnesium. Reducing sodium intake may drop your blood pressure a few points, but it doesn’t translate to better cardiovascular health.

 

References

Are You Still Restricting Salt?

I was planning on writing about the current salt and sodium recommendations and the lack of solid research supporting them, but I realized that there are already enough comprehensive articles written about that (like this one). Instead, I’ll quickly summarize the absurdity of the current sodium recommendations and focus on the problems caused by restricting salt.

 

Some Ridiculous Guidelines

The current Dietary Guidelines for Americans recommend that we consume less than 2,300 mg sodium per day and less than 1,500 mg sodium for individuals with high blood pressure (1), the World Health Organization recommends that we consume less than 2,000 mg sodium per day (2), and the American Heart Association recommends an ideal limit of no more than 1,500 mg sodium per day for most adults (3).

These recommendations are aimed at reducing hypertension and cardiovascular disease. However, they’re at odds with much of the research, which shows that the current sodium recommendations are between 2 and 4 times lower than what is ideal for cardiovascular health and health in general.

Sodium intakes of 4,000-6,000 mg per day are associated with the lowest risk of cardiovascular death and hospitalization for congestive heart failure (4) while consuming under 2,300 mg sodium per day is associated with increased cardiovascular disease mortality and all-cause mortality (5). And, even consuming less than 3,600 mg per day is associated with greater cardiovascular disease mortality (6).

 

Sodium, the (Almost) Perfect Scapegoat

Ridiculous recommendations aside, sodium is an extraordinarily important mineral that has been wrongly blamed for causing hypertension and cardiovascular disease. This blame comes primarily from sodium’s ability to attract water.

When we consume sodium, the amount of sodium in our blood increases, which increases our blood volume because sodium attracts water.

Our blood pressure is a function of the volume of blood in circulation and the constriction or relaxation of our blood vessels. When our blood volume increases or blood vessels constrict, our blood pressure increases, and vice versa.

So, it’s assumed that increasing sodium consumption increases blood pressure by increasing the blood volume. It’s then assumed that this high blood pressure leads to cardiovascular disease. By the same line of thinking, sodium is blamed for increasing swelling, bloating, and water retention due to its attraction for water.

But, like the “calories-in versus calories-out” model of fat loss, these ideas are based on oversimplified models of the human body that ignore that we adapt to our environments.

When the blood volume is increased from increased salt consumption, our bodies adapt by increasing the amount of sodium they excrete and relaxing our blood vessels. This allows us to maintain a relatively steady blood pressure, while also allowing for optimal blood flow, mineral balance, and energy production. This is easier to explain by describing what happens when we don’t consume enough sodium.

 

What Happens When We Don’t Consume Enough Salt?

Contrary to the mainstream ideas, a low salt intake actually contributes to poor cardiovascular health and swelling and bloating.

When we reduce our salt intake, the amount of sodium in the blood is reduced, which causes an immediate reduction in blood volume and blood pressure. This is why reducing salt intake is suggested for reducing high blood pressure.

But it doesn’t end there.

Maintaining adequate blood pressure is extremely important for transporting nutrients and waste throughout our bodies. So, when our blood pressure is acutely reduced, our stress systems are activated in response (7).

Our stress systems constrict our blood vessels and release the stress hormone aldosterone, which reduces the amount of sodium that we excrete in our kidneys, allowing us to maintain higher sodium (and water) levels in our blood (8). This keeps our blood volume and blood pressure at the levels needed to transport nutrients and waste throughout the body.

But, while this balancing act allows us to maintain blood volume and blood pressure in the short term, it comes at a cost: the sodium we would normally excrete in our kidneys is replaced with potassium and magnesium (9). This means that when we reduce our salt consumption, we lose greater amounts of potassium and magnesium.

Like other adaptive processes, this isn’t a problem in acute situations. But when continued chronically, losing potassium and magnesium can contribute to high blood pressure and inhibit our bodies’ ability to produce energy.

 

Sodium, Swelling, and Energy Production

Potassium and magnesium are balanced with sodium in the cellular environment. Potassium and magnesium are housed within our cells, while sodium remains outside of the cell. This also keeps water outside of the cells (with sodium), which is an important feature of a healthy cell.

When we lose potassium and magnesium due to a low sodium intake, there is less potassium and magnesium in our cells. This then allows more sodium to enter the cell, bringing water with it, which causes the cell to swell (10). The increase in aldosterone due to a low sodium intake also contributes to this cell swelling (11, 12, 13).

This swelling is a real problem – a swollen cell can’t properly produce or use energy (14). Not only is this disastrous for our metabolism, which lies at the foundation of our health, but it can also contribute to cardiovascular problems!

When the cells in our blood vessels swell due to their lack of potassium and magnesium, it inhibits their ability to relax and causes our blood vessels to constrict (like a swollen muscle after working out) (15, 16, 17). This helps to make up for the reduced blood volume from less salt consumption, but also restricts blood flow throughout our bodies and can cause other cardiovascular problems.

In other words, when we eat less salt, our blood pressure is maintained via our stress systems. But, when this occurs over time, we lose potassium and magnesium, leading to cell swelling that inhibits energy production and can cause cardiovascular problems.

 

How Much Salt Should We Eat?

Eating too little salt increases stress, reduces the metabolism, and can lead to cardiovascular problems in the long-term (7, 18, 19).

On the other hand, consuming enough salt allows for optimal energy production, adequate blood volume, reduced swelling and bloating, and sparing of potassium and magnesium. This allows for proper metabolic function, cardiovascular function, and really all other functions.

So, should we eat salt to our heart’s content?

Pretty much! Our sense of taste has been designed to dictate our nutrient intake. When we don’t have enough sodium, we have a stronger desire to eat salty foods, and vice versa (20). So, we can just listen to what our bodies need and allow that to dictate how much salt we consume.

In other words, salt to taste!

If you’re worried about your blood pressure, then make sure you’re getting enough potassium and magnesium. Reducing sodium intake may drop your blood pressure a few points, but it doesn’t translate to better cardiovascular health.

 

References

Are You Still Restricting Salt?

I was planning on writing about the current salt and sodium recommendations and the lack of solid research supporting them, but I realized that there are already enough comprehensive articles written about that (like this one). Instead, I’ll quickly summarize the absurdity of the current sodium recommendations and focus on the problems caused by restricting salt.

 

Some Ridiculous Guidelines

The current Dietary Guidelines for Americans recommend that we consume less than 2,300 mg sodium per day and less than 1,500 mg sodium for individuals with high blood pressure (1), the World Health Organization recommends that we consume less than 2,000 mg sodium per day (2), and the American Heart Association recommends an ideal limit of no more than 1,500 mg sodium per day for most adults (3).

These recommendations are aimed at reducing hypertension and cardiovascular disease. However, they’re at odds with much of the research, which shows that the current sodium recommendations are between 2 and 4 times lower than what is ideal for cardiovascular health and health in general.

Sodium intakes of 4,000-6,000 mg per day are associated with the lowest risk of cardiovascular death and hospitalization for congestive heart failure (4) while consuming under 2,300 mg sodium per day is associated with increased cardiovascular disease mortality and all-cause mortality (5). And, even consuming less than 3,600 mg per day is associated with greater cardiovascular disease mortality (6).

 

Sodium, the (Almost) Perfect Scapegoat

Ridiculous recommendations aside, sodium is an extraordinarily important mineral that has been wrongly blamed for causing hypertension and cardiovascular disease. This blame comes primarily from sodium’s ability to attract water.

When we consume sodium, the amount of sodium in our blood increases, which increases our blood volume because sodium attracts water.

Our blood pressure is a function of the volume of blood in circulation and the constriction or relaxation of our blood vessels. When our blood volume increases or blood vessels constrict, our blood pressure increases, and vice versa.

So, it’s assumed that increasing sodium consumption increases blood pressure by increasing the blood volume. It’s then assumed that this high blood pressure leads to cardiovascular disease. By the same line of thinking, sodium is blamed for increasing swelling, bloating, and water retention due to its attraction for water.

But, like the “calories-in versus calories-out” model of fat loss, these ideas are based on oversimplified models of the human body that ignore that we adapt to our environments.

When the blood volume is increased from increased salt consumption, our bodies adapt by increasing the amount of sodium they excrete and relaxing our blood vessels. This allows us to maintain a relatively steady blood pressure, while also allowing for optimal blood flow, mineral balance, and energy production. This is easier to explain by describing what happens when we don’t consume enough sodium.

 

What Happens When We Don’t Consume Enough Salt?

Contrary to the mainstream ideas, a low salt intake actually contributes to poor cardiovascular health and swelling and bloating.

When we reduce our salt intake, the amount of sodium in the blood is reduced, which causes an immediate reduction in blood volume and blood pressure. This is why reducing salt intake is suggested for reducing high blood pressure.

But it doesn’t end there.

Maintaining adequate blood pressure is extremely important for transporting nutrients and waste throughout our bodies. So, when our blood pressure is acutely reduced, our stress systems are activated in response (7).

Our stress systems constrict our blood vessels and release the stress hormone aldosterone, which reduces the amount of sodium that we excrete in our kidneys, allowing us to maintain higher sodium (and water) levels in our blood (8). This keeps our blood volume and blood pressure at the levels needed to transport nutrients and waste throughout the body.

But, while this balancing act allows us to maintain blood volume and blood pressure in the short term, it comes at a cost: the sodium we would normally excrete in our kidneys is replaced with potassium and magnesium (9). This means that when we reduce our salt consumption, we lose greater amounts of potassium and magnesium.

Like other adaptive processes, this isn’t a problem in acute situations. But when continued chronically, losing potassium and magnesium can contribute to high blood pressure and inhibit our bodies’ ability to produce energy.

 

Sodium, Swelling, and Energy Production

Potassium and magnesium are balanced with sodium in the cellular environment. Potassium and magnesium are housed within our cells, while sodium remains outside of the cell. This also keeps water outside of the cells (with sodium), which is an important feature of a healthy cell.

When we lose potassium and magnesium due to a low sodium intake, there is less potassium and magnesium in our cells. This then allows more sodium to enter the cell, bringing water with it, which causes the cell to swell (10). The increase in aldosterone due to a low sodium intake also contributes to this cell swelling (11, 12, 13).

This swelling is a real problem – a swollen cell can’t properly produce or use energy (14). Not only is this disastrous for our metabolism, which lies at the foundation of our health, but it can also contribute to cardiovascular problems!

When the cells in our blood vessels swell due to their lack of potassium and magnesium, it inhibits their ability to relax and causes our blood vessels to constrict (like a swollen muscle after working out) (15, 16, 17). This helps to make up for the reduced blood volume from less salt consumption, but also restricts blood flow throughout our bodies and can cause other cardiovascular problems.

In other words, when we eat less salt, our blood pressure is maintained via our stress systems. But, when this occurs over time, we lose potassium and magnesium, leading to cell swelling that inhibits energy production and can cause cardiovascular problems.

 

How Much Salt Should We Eat?

Eating too little salt increases stress, reduces the metabolism, and can lead to cardiovascular problems in the long-term (7, 18, 19).

On the other hand, consuming enough salt allows for optimal energy production, adequate blood volume, reduced swelling and bloating, and sparing of potassium and magnesium. This allows for proper metabolic function, cardiovascular function, and really all other functions.

So, should we eat salt to our heart’s content?

Pretty much! Our sense of taste has been designed to dictate our nutrient intake. When we don’t have enough sodium, we have a stronger desire to eat salty foods, and vice versa (20). So, we can just listen to what our bodies need and allow that to dictate how much salt we consume.

In other words, salt to taste!

If you’re worried about your blood pressure, then make sure you’re getting enough potassium and magnesium. Reducing sodium intake may drop your blood pressure a few points, but it doesn’t translate to better cardiovascular health.

 

References

Are You Still Restricting Salt?

I was planning on writing about the current salt and sodium recommendations and the lack of solid research supporting them, but I realized that there are already enough comprehensive articles written about that (like this one). Instead, I’ll quickly summarize the absurdity of the current sodium recommendations and focus on the problems caused by restricting salt.

 

Some Ridiculous Guidelines

The current Dietary Guidelines for Americans recommend that we consume less than 2,300 mg sodium per day and less than 1,500 mg sodium for individuals with high blood pressure (1), the World Health Organization recommends that we consume less than 2,000 mg sodium per day (2), and the American Heart Association recommends an ideal limit of no more than 1,500 mg sodium per day for most adults (3).

These recommendations are aimed at reducing hypertension and cardiovascular disease. However, they’re at odds with much of the research, which shows that the current sodium recommendations are between 2 and 4 times lower than what is ideal for cardiovascular health and health in general.

Sodium intakes of 4,000-6,000 mg per day are associated with the lowest risk of cardiovascular death and hospitalization for congestive heart failure (4) while consuming under 2,300 mg sodium per day is associated with increased cardiovascular disease mortality and all-cause mortality (5). And, even consuming less than 3,600 mg per day is associated with greater cardiovascular disease mortality (6).

 

Sodium, the (Almost) Perfect Scapegoat

Ridiculous recommendations aside, sodium is an extraordinarily important mineral that has been wrongly blamed for causing hypertension and cardiovascular disease. This blame comes primarily from sodium’s ability to attract water.

When we consume sodium, the amount of sodium in our blood increases, which increases our blood volume because sodium attracts water.

Our blood pressure is a function of the volume of blood in circulation and the constriction or relaxation of our blood vessels. When our blood volume increases or blood vessels constrict, our blood pressure increases, and vice versa.

So, it’s assumed that increasing sodium consumption increases blood pressure by increasing the blood volume. It’s then assumed that this high blood pressure leads to cardiovascular disease. By the same line of thinking, sodium is blamed for increasing swelling, bloating, and water retention due to its attraction for water.

But, like the “calories-in versus calories-out” model of fat loss, these ideas are based on oversimplified models of the human body that ignore that we adapt to our environments.

When the blood volume is increased from increased salt consumption, our bodies adapt by increasing the amount of sodium they excrete and relaxing our blood vessels. This allows us to maintain a relatively steady blood pressure, while also allowing for optimal blood flow, mineral balance, and energy production. This is easier to explain by describing what happens when we don’t consume enough sodium.

 

What Happens When We Don’t Consume Enough Salt?

Contrary to the mainstream ideas, a low salt intake actually contributes to poor cardiovascular health and swelling and bloating.

When we reduce our salt intake, the amount of sodium in the blood is reduced, which causes an immediate reduction in blood volume and blood pressure. This is why reducing salt intake is suggested for reducing high blood pressure.

But it doesn’t end there.

Maintaining adequate blood pressure is extremely important for transporting nutrients and waste throughout our bodies. So, when our blood pressure is acutely reduced, our stress systems are activated in response (7).

Our stress systems constrict our blood vessels and release the stress hormone aldosterone, which reduces the amount of sodium that we excrete in our kidneys, allowing us to maintain higher sodium (and water) levels in our blood (8). This keeps our blood volume and blood pressure at the levels needed to transport nutrients and waste throughout the body.

But, while this balancing act allows us to maintain blood volume and blood pressure in the short term, it comes at a cost: the sodium we would normally excrete in our kidneys is replaced with potassium and magnesium (9). This means that when we reduce our salt consumption, we lose greater amounts of potassium and magnesium.

Like other adaptive processes, this isn’t a problem in acute situations. But when continued chronically, losing potassium and magnesium can contribute to high blood pressure and inhibit our bodies’ ability to produce energy.

 

Sodium, Swelling, and Energy Production

Potassium and magnesium are balanced with sodium in the cellular environment. Potassium and magnesium are housed within our cells, while sodium remains outside of the cell. This also keeps water outside of the cells (with sodium), which is an important feature of a healthy cell.

When we lose potassium and magnesium due to a low sodium intake, there is less potassium and magnesium in our cells. This then allows more sodium to enter the cell, bringing water with it, which causes the cell to swell (10). The increase in aldosterone due to a low sodium intake also contributes to this cell swelling (11, 12, 13).

This swelling is a real problem – a swollen cell can’t properly produce or use energy (14). Not only is this disastrous for our metabolism, which lies at the foundation of our health, but it can also contribute to cardiovascular problems!

When the cells in our blood vessels swell due to their lack of potassium and magnesium, it inhibits their ability to relax and causes our blood vessels to constrict (like a swollen muscle after working out) (15, 16, 17). This helps to make up for the reduced blood volume from less salt consumption, but also restricts blood flow throughout our bodies and can cause other cardiovascular problems.

In other words, when we eat less salt, our blood pressure is maintained via our stress systems. But, when this occurs over time, we lose potassium and magnesium, leading to cell swelling that inhibits energy production and can cause cardiovascular problems.

 

How Much Salt Should We Eat?

Eating too little salt increases stress, reduces the metabolism, and can lead to cardiovascular problems in the long-term (7, 18, 19).

On the other hand, consuming enough salt allows for optimal energy production, adequate blood volume, reduced swelling and bloating, and sparing of potassium and magnesium. This allows for proper metabolic function, cardiovascular function, and really all other functions.

So, should we eat salt to our heart’s content?

Pretty much! Our sense of taste has been designed to dictate our nutrient intake. When we don’t have enough sodium, we have a stronger desire to eat salty foods, and vice versa (20). So, we can just listen to what our bodies need and allow that to dictate how much salt we consume.

In other words, salt to taste!

If you’re worried about your blood pressure, then make sure you’re getting enough potassium and magnesium. Reducing sodium intake may drop your blood pressure a few points, but it doesn’t translate to better cardiovascular health.

 

References

Are You Still Restricting Salt?

I was planning on writing about the current salt and sodium recommendations and the lack of solid research supporting them, but I realized that there are already enough comprehensive articles written about that (like this one). Instead, I’ll quickly summarize the absurdity of the current sodium recommendations and focus on the problems caused by restricting salt.

 

Some Ridiculous Guidelines

The current Dietary Guidelines for Americans recommend that we consume less than 2,300 mg sodium per day and less than 1,500 mg sodium for individuals with high blood pressure (1), the World Health Organization recommends that we consume less than 2,000 mg sodium per day (2), and the American Heart Association recommends an ideal limit of no more than 1,500 mg sodium per day for most adults (3).

These recommendations are aimed at reducing hypertension and cardiovascular disease. However, they’re at odds with much of the research, which shows that the current sodium recommendations are between 2 and 4 times lower than what is ideal for cardiovascular health and health in general.

Sodium intakes of 4,000-6,000 mg per day are associated with the lowest risk of cardiovascular death and hospitalization for congestive heart failure (4) while consuming under 2,300 mg sodium per day is associated with increased cardiovascular disease mortality and all-cause mortality (5). And, even consuming less than 3,600 mg per day is associated with greater cardiovascular disease mortality (6).

 

Sodium, the (Almost) Perfect Scapegoat

Ridiculous recommendations aside, sodium is an extraordinarily important mineral that has been wrongly blamed for causing hypertension and cardiovascular disease. This blame comes primarily from sodium’s ability to attract water.

When we consume sodium, the amount of sodium in our blood increases, which increases our blood volume because sodium attracts water.

Our blood pressure is a function of the volume of blood in circulation and the constriction or relaxation of our blood vessels. When our blood volume increases or blood vessels constrict, our blood pressure increases, and vice versa.

So, it’s assumed that increasing sodium consumption increases blood pressure by increasing the blood volume. It’s then assumed that this high blood pressure leads to cardiovascular disease. By the same line of thinking, sodium is blamed for increasing swelling, bloating, and water retention due to its attraction for water.

But, like the “calories-in versus calories-out” model of fat loss, these ideas are based on oversimplified models of the human body that ignore that we adapt to our environments.

When the blood volume is increased from increased salt consumption, our bodies adapt by increasing the amount of sodium they excrete and relaxing our blood vessels. This allows us to maintain a relatively steady blood pressure, while also allowing for optimal blood flow, mineral balance, and energy production. This is easier to explain by describing what happens when we don’t consume enough sodium.

 

What Happens When We Don’t Consume Enough Salt?

Contrary to the mainstream ideas, a low salt intake actually contributes to poor cardiovascular health and swelling and bloating.

When we reduce our salt intake, the amount of sodium in the blood is reduced, which causes an immediate reduction in blood volume and blood pressure. This is why reducing salt intake is suggested for reducing high blood pressure.

But it doesn’t end there.

Maintaining adequate blood pressure is extremely important for transporting nutrients and waste throughout our bodies. So, when our blood pressure is acutely reduced, our stress systems are activated in response (7).

Our stress systems constrict our blood vessels and release the stress hormone aldosterone, which reduces the amount of sodium that we excrete in our kidneys, allowing us to maintain higher sodium (and water) levels in our blood (8). This keeps our blood volume and blood pressure at the levels needed to transport nutrients and waste throughout the body.

But, while this balancing act allows us to maintain blood volume and blood pressure in the short term, it comes at a cost: the sodium we would normally excrete in our kidneys is replaced with potassium and magnesium (9). This means that when we reduce our salt consumption, we lose greater amounts of potassium and magnesium.

Like other adaptive processes, this isn’t a problem in acute situations. But when continued chronically, losing potassium and magnesium can contribute to high blood pressure and inhibit our bodies’ ability to produce energy.

 

Sodium, Swelling, and Energy Production

Potassium and magnesium are balanced with sodium in the cellular environment. Potassium and magnesium are housed within our cells, while sodium remains outside of the cell. This also keeps water outside of the cells (with sodium), which is an important feature of a healthy cell.

When we lose potassium and magnesium due to a low sodium intake, there is less potassium and magnesium in our cells. This then allows more sodium to enter the cell, bringing water with it, which causes the cell to swell (10). The increase in aldosterone due to a low sodium intake also contributes to this cell swelling (11, 12, 13).

This swelling is a real problem – a swollen cell can’t properly produce or use energy (14). Not only is this disastrous for our metabolism, which lies at the foundation of our health, but it can also contribute to cardiovascular problems!

When the cells in our blood vessels swell due to their lack of potassium and magnesium, it inhibits their ability to relax and causes our blood vessels to constrict (like a swollen muscle after working out) (15, 16, 17). This helps to make up for the reduced blood volume from less salt consumption, but also restricts blood flow throughout our bodies and can cause other cardiovascular problems.

In other words, when we eat less salt, our blood pressure is maintained via our stress systems. But, when this occurs over time, we lose potassium and magnesium, leading to cell swelling that inhibits energy production and can cause cardiovascular problems.

 

How Much Salt Should We Eat?

Eating too little salt increases stress, reduces the metabolism, and can lead to cardiovascular problems in the long-term (7, 18, 19).

On the other hand, consuming enough salt allows for optimal energy production, adequate blood volume, reduced swelling and bloating, and sparing of potassium and magnesium. This allows for proper metabolic function, cardiovascular function, and really all other functions.

So, should we eat salt to our heart’s content?

Pretty much! Our sense of taste has been designed to dictate our nutrient intake. When we don’t have enough sodium, we have a stronger desire to eat salty foods, and vice versa (20). So, we can just listen to what our bodies need and allow that to dictate how much salt we consume.

In other words, salt to taste!

If you’re worried about your blood pressure, then make sure you’re getting enough potassium and magnesium. Reducing sodium intake may drop your blood pressure a few points, but it doesn’t translate to better cardiovascular health.

 

References

Are You Still Restricting Salt?

I was planning on writing about the current salt and sodium recommendations and the lack of solid research supporting them, but I realized that there are already enough comprehensive articles written about that (like this one). Instead, I’ll quickly summarize the absurdity of the current sodium recommendations and focus on the problems caused by restricting salt.

 

Some Ridiculous Guidelines

The current Dietary Guidelines for Americans recommend that we consume less than 2,300 mg sodium per day and less than 1,500 mg sodium for individuals with high blood pressure (1), the World Health Organization recommends that we consume less than 2,000 mg sodium per day (2), and the American Heart Association recommends an ideal limit of no more than 1,500 mg sodium per day for most adults (3).

These recommendations are aimed at reducing hypertension and cardiovascular disease. However, they’re at odds with much of the research, which shows that the current sodium recommendations are between 2 and 4 times lower than what is ideal for cardiovascular health and health in general.

Sodium intakes of 4,000-6,000 mg per day are associated with the lowest risk of cardiovascular death and hospitalization for congestive heart failure (4) while consuming under 2,300 mg sodium per day is associated with increased cardiovascular disease mortality and all-cause mortality (5). And, even consuming less than 3,600 mg per day is associated with greater cardiovascular disease mortality (6).

 

Sodium, the (Almost) Perfect Scapegoat

Ridiculous recommendations aside, sodium is an extraordinarily important mineral that has been wrongly blamed for causing hypertension and cardiovascular disease. This blame comes primarily from sodium’s ability to attract water.

When we consume sodium, the amount of sodium in our blood increases, which increases our blood volume because sodium attracts water.

Our blood pressure is a function of the volume of blood in circulation and the constriction or relaxation of our blood vessels. When our blood volume increases or blood vessels constrict, our blood pressure increases, and vice versa.

So, it’s assumed that increasing sodium consumption increases blood pressure by increasing the blood volume. It’s then assumed that this high blood pressure leads to cardiovascular disease. By the same line of thinking, sodium is blamed for increasing swelling, bloating, and water retention due to its attraction for water.

But, like the “calories-in versus calories-out” model of fat loss, these ideas are based on oversimplified models of the human body that ignore that we adapt to our environments.

When the blood volume is increased from increased salt consumption, our bodies adapt by increasing the amount of sodium they excrete and relaxing our blood vessels. This allows us to maintain a relatively steady blood pressure, while also allowing for optimal blood flow, mineral balance, and energy production. This is easier to explain by describing what happens when we don’t consume enough sodium.

 

What Happens When We Don’t Consume Enough Salt?

Contrary to the mainstream ideas, a low salt intake actually contributes to poor cardiovascular health and swelling and bloating.

When we reduce our salt intake, the amount of sodium in the blood is reduced, which causes an immediate reduction in blood volume and blood pressure. This is why reducing salt intake is suggested for reducing high blood pressure.

But it doesn’t end there.

Maintaining adequate blood pressure is extremely important for transporting nutrients and waste throughout our bodies. So, when our blood pressure is acutely reduced, our stress systems are activated in response (7).

Our stress systems constrict our blood vessels and release the stress hormone aldosterone, which reduces the amount of sodium that we excrete in our kidneys, allowing us to maintain higher sodium (and water) levels in our blood (8). This keeps our blood volume and blood pressure at the levels needed to transport nutrients and waste throughout the body.

But, while this balancing act allows us to maintain blood volume and blood pressure in the short term, it comes at a cost: the sodium we would normally excrete in our kidneys is replaced with potassium and magnesium (9). This means that when we reduce our salt consumption, we lose greater amounts of potassium and magnesium.

Like other adaptive processes, this isn’t a problem in acute situations. But when continued chronically, losing potassium and magnesium can contribute to high blood pressure and inhibit our bodies’ ability to produce energy.

 

Sodium, Swelling, and Energy Production

Potassium and magnesium are balanced with sodium in the cellular environment. Potassium and magnesium are housed within our cells, while sodium remains outside of the cell. This also keeps water outside of the cells (with sodium), which is an important feature of a healthy cell.

When we lose potassium and magnesium due to a low sodium intake, there is less potassium and magnesium in our cells. This then allows more sodium to enter the cell, bringing water with it, which causes the cell to swell (10). The increase in aldosterone due to a low sodium intake also contributes to this cell swelling (11, 12, 13).

This swelling is a real problem – a swollen cell can’t properly produce or use energy (14). Not only is this disastrous for our metabolism, which lies at the foundation of our health, but it can also contribute to cardiovascular problems!

When the cells in our blood vessels swell due to their lack of potassium and magnesium, it inhibits their ability to relax and causes our blood vessels to constrict (like a swollen muscle after working out) (15, 16, 17). This helps to make up for the reduced blood volume from less salt consumption, but also restricts blood flow throughout our bodies and can cause other cardiovascular problems.

In other words, when we eat less salt, our blood pressure is maintained via our stress systems. But, when this occurs over time, we lose potassium and magnesium, leading to cell swelling that inhibits energy production and can cause cardiovascular problems.

 

How Much Salt Should We Eat?

Eating too little salt increases stress, reduces the metabolism, and can lead to cardiovascular problems in the long-term (7, 18, 19).

On the other hand, consuming enough salt allows for optimal energy production, adequate blood volume, reduced swelling and bloating, and sparing of potassium and magnesium. This allows for proper metabolic function, cardiovascular function, and really all other functions.

So, should we eat salt to our heart’s content?

Pretty much! Our sense of taste has been designed to dictate our nutrient intake. When we don’t have enough sodium, we have a stronger desire to eat salty foods, and vice versa (20). So, we can just listen to what our bodies need and allow that to dictate how much salt we consume.

In other words, salt to taste!

If you’re worried about your blood pressure, then make sure you’re getting enough potassium and magnesium. Reducing sodium intake may drop your blood pressure a few points, but it doesn’t translate to better cardiovascular health.

 

References

Are You Still Restricting Salt?

I was planning on writing about the current salt and sodium recommendations and the lack of solid research supporting them, but I realized that there are already enough comprehensive articles written about that (like this one). Instead, I’ll quickly summarize the absurdity of the current sodium recommendations and focus on the problems caused by restricting salt.

 

Some Ridiculous Guidelines

The current Dietary Guidelines for Americans recommend that we consume less than 2,300 mg sodium per day and less than 1,500 mg sodium for individuals with high blood pressure (1), the World Health Organization recommends that we consume less than 2,000 mg sodium per day (2), and the American Heart Association recommends an ideal limit of no more than 1,500 mg sodium per day for most adults (3).

These recommendations are aimed at reducing hypertension and cardiovascular disease. However, they’re at odds with much of the research, which shows that the current sodium recommendations are between 2 and 4 times lower than what is ideal for cardiovascular health and health in general.

Sodium intakes of 4,000-6,000 mg per day are associated with the lowest risk of cardiovascular death and hospitalization for congestive heart failure (4) while consuming under 2,300 mg sodium per day is associated with increased cardiovascular disease mortality and all-cause mortality (5). And, even consuming less than 3,600 mg per day is associated with greater cardiovascular disease mortality (6).

 

Sodium, the (Almost) Perfect Scapegoat

Ridiculous recommendations aside, sodium is an extraordinarily important mineral that has been wrongly blamed for causing hypertension and cardiovascular disease. This blame comes primarily from sodium’s ability to attract water.

When we consume sodium, the amount of sodium in our blood increases, which increases our blood volume because sodium attracts water.

Our blood pressure is a function of the volume of blood in circulation and the constriction or relaxation of our blood vessels. When our blood volume increases or blood vessels constrict, our blood pressure increases, and vice versa.

So, it’s assumed that increasing sodium consumption increases blood pressure by increasing the blood volume. It’s then assumed that this high blood pressure leads to cardiovascular disease. By the same line of thinking, sodium is blamed for increasing swelling, bloating, and water retention due to its attraction for water.

But, like the “calories-in versus calories-out” model of fat loss, these ideas are based on oversimplified models of the human body that ignore that we adapt to our environments.

When the blood volume is increased from increased salt consumption, our bodies adapt by increasing the amount of sodium they excrete and relaxing our blood vessels. This allows us to maintain a relatively steady blood pressure, while also allowing for optimal blood flow, mineral balance, and energy production. This is easier to explain by describing what happens when we don’t consume enough sodium.

 

What Happens When We Don’t Consume Enough Salt?

Contrary to the mainstream ideas, a low salt intake actually contributes to poor cardiovascular health and swelling and bloating.

When we reduce our salt intake, the amount of sodium in the blood is reduced, which causes an immediate reduction in blood volume and blood pressure. This is why reducing salt intake is suggested for reducing high blood pressure.

But it doesn’t end there.

Maintaining adequate blood pressure is extremely important for transporting nutrients and waste throughout our bodies. So, when our blood pressure is acutely reduced, our stress systems are activated in response (7).

Our stress systems constrict our blood vessels and release the stress hormone aldosterone, which reduces the amount of sodium that we excrete in our kidneys, allowing us to maintain higher sodium (and water) levels in our blood (8). This keeps our blood volume and blood pressure at the levels needed to transport nutrients and waste throughout the body.

But, while this balancing act allows us to maintain blood volume and blood pressure in the short term, it comes at a cost: the sodium we would normally excrete in our kidneys is replaced with potassium and magnesium (9). This means that when we reduce our salt consumption, we lose greater amounts of potassium and magnesium.

Like other adaptive processes, this isn’t a problem in acute situations. But when continued chronically, losing potassium and magnesium can contribute to high blood pressure and inhibit our bodies’ ability to produce energy.

 

Sodium, Swelling, and Energy Production

Potassium and magnesium are balanced with sodium in the cellular environment. Potassium and magnesium are housed within our cells, while sodium remains outside of the cell. This also keeps water outside of the cells (with sodium), which is an important feature of a healthy cell.

When we lose potassium and magnesium due to a low sodium intake, there is less potassium and magnesium in our cells. This then allows more sodium to enter the cell, bringing water with it, which causes the cell to swell (10). The increase in aldosterone due to a low sodium intake also contributes to this cell swelling (11, 12, 13).

This swelling is a real problem – a swollen cell can’t properly produce or use energy (14). Not only is this disastrous for our metabolism, which lies at the foundation of our health, but it can also contribute to cardiovascular problems!

When the cells in our blood vessels swell due to their lack of potassium and magnesium, it inhibits their ability to relax and causes our blood vessels to constrict (like a swollen muscle after working out) (15, 16, 17). This helps to make up for the reduced blood volume from less salt consumption, but also restricts blood flow throughout our bodies and can cause other cardiovascular problems.

In other words, when we eat less salt, our blood pressure is maintained via our stress systems. But, when this occurs over time, we lose potassium and magnesium, leading to cell swelling that inhibits energy production and can cause cardiovascular problems.

 

How Much Salt Should We Eat?

Eating too little salt increases stress, reduces the metabolism, and can lead to cardiovascular problems in the long-term (7, 18, 19).

On the other hand, consuming enough salt allows for optimal energy production, adequate blood volume, reduced swelling and bloating, and sparing of potassium and magnesium. This allows for proper metabolic function, cardiovascular function, and really all other functions.

So, should we eat salt to our heart’s content?

Pretty much! Our sense of taste has been designed to dictate our nutrient intake. When we don’t have enough sodium, we have a stronger desire to eat salty foods, and vice versa (20). So, we can just listen to what our bodies need and allow that to dictate how much salt we consume.

In other words, salt to taste!

If you’re worried about your blood pressure, then make sure you’re getting enough potassium and magnesium. Reducing sodium intake may drop your blood pressure a few points, but it doesn’t translate to better cardiovascular health.

 

References

Are You Still Restricting Salt?

I was planning on writing about the current salt and sodium recommendations and the lack of solid research supporting them, but I realized that there are already enough comprehensive articles written about that (like this one). Instead, I’ll quickly summarize the absurdity of the current sodium recommendations and focus on the problems caused by restricting salt.

 

Some Ridiculous Guidelines

The current Dietary Guidelines for Americans recommend that we consume less than 2,300 mg sodium per day and less than 1,500 mg sodium for individuals with high blood pressure (1), the World Health Organization recommends that we consume less than 2,000 mg sodium per day (2), and the American Heart Association recommends an ideal limit of no more than 1,500 mg sodium per day for most adults (3).

These recommendations are aimed at reducing hypertension and cardiovascular disease. However, they’re at odds with much of the research, which shows that the current sodium recommendations are between 2 and 4 times lower than what is ideal for cardiovascular health and health in general.

Sodium intakes of 4,000-6,000 mg per day are associated with the lowest risk of cardiovascular death and hospitalization for congestive heart failure (4) while consuming under 2,300 mg sodium per day is associated with increased cardiovascular disease mortality and all-cause mortality (5). And, even consuming less than 3,600 mg per day is associated with greater cardiovascular disease mortality (6).

 

Sodium, the (Almost) Perfect Scapegoat

Ridiculous recommendations aside, sodium is an extraordinarily important mineral that has been wrongly blamed for causing hypertension and cardiovascular disease. This blame comes primarily from sodium’s ability to attract water.

When we consume sodium, the amount of sodium in our blood increases, which increases our blood volume because sodium attracts water.

Our blood pressure is a function of the volume of blood in circulation and the constriction or relaxation of our blood vessels. When our blood volume increases or blood vessels constrict, our blood pressure increases, and vice versa.

So, it’s assumed that increasing sodium consumption increases blood pressure by increasing the blood volume. It’s then assumed that this high blood pressure leads to cardiovascular disease. By the same line of thinking, sodium is blamed for increasing swelling, bloating, and water retention due to its attraction for water.

But, like the “calories-in versus calories-out” model of fat loss, these ideas are based on oversimplified models of the human body that ignore that we adapt to our environments.

When the blood volume is increased from increased salt consumption, our bodies adapt by increasing the amount of sodium they excrete and relaxing our blood vessels. This allows us to maintain a relatively steady blood pressure, while also allowing for optimal blood flow, mineral balance, and energy production. This is easier to explain by describing what happens when we don’t consume enough sodium.

 

What Happens When We Don’t Consume Enough Salt?

Contrary to the mainstream ideas, a low salt intake actually contributes to poor cardiovascular health and swelling and bloating.

When we reduce our salt intake, the amount of sodium in the blood is reduced, which causes an immediate reduction in blood volume and blood pressure. This is why reducing salt intake is suggested for reducing high blood pressure.

But it doesn’t end there.

Maintaining adequate blood pressure is extremely important for transporting nutrients and waste throughout our bodies. So, when our blood pressure is acutely reduced, our stress systems are activated in response (7).

Our stress systems constrict our blood vessels and release the stress hormone aldosterone, which reduces the amount of sodium that we excrete in our kidneys, allowing us to maintain higher sodium (and water) levels in our blood (8). This keeps our blood volume and blood pressure at the levels needed to transport nutrients and waste throughout the body.

But, while this balancing act allows us to maintain blood volume and blood pressure in the short term, it comes at a cost: the sodium we would normally excrete in our kidneys is replaced with potassium and magnesium (9). This means that when we reduce our salt consumption, we lose greater amounts of potassium and magnesium.

Like other adaptive processes, this isn’t a problem in acute situations. But when continued chronically, losing potassium and magnesium can contribute to high blood pressure and inhibit our bodies’ ability to produce energy.

 

Sodium, Swelling, and Energy Production

Potassium and magnesium are balanced with sodium in the cellular environment. Potassium and magnesium are housed within our cells, while sodium remains outside of the cell. This also keeps water outside of the cells (with sodium), which is an important feature of a healthy cell.

When we lose potassium and magnesium due to a low sodium intake, there is less potassium and magnesium in our cells. This then allows more sodium to enter the cell, bringing water with it, which causes the cell to swell (10). The increase in aldosterone due to a low sodium intake also contributes to this cell swelling (11, 12, 13).

This swelling is a real problem – a swollen cell can’t properly produce or use energy (14). Not only is this disastrous for our metabolism, which lies at the foundation of our health, but it can also contribute to cardiovascular problems!

When the cells in our blood vessels swell due to their lack of potassium and magnesium, it inhibits their ability to relax and causes our blood vessels to constrict (like a swollen muscle after working out) (15, 16, 17). This helps to make up for the reduced blood volume from less salt consumption, but also restricts blood flow throughout our bodies and can cause other cardiovascular problems.

In other words, when we eat less salt, our blood pressure is maintained via our stress systems. But, when this occurs over time, we lose potassium and magnesium, leading to cell swelling that inhibits energy production and can cause cardiovascular problems.

 

How Much Salt Should We Eat?

Eating too little salt increases stress, reduces the metabolism, and can lead to cardiovascular problems in the long-term (7, 18, 19).

On the other hand, consuming enough salt allows for optimal energy production, adequate blood volume, reduced swelling and bloating, and sparing of potassium and magnesium. This allows for proper metabolic function, cardiovascular function, and really all other functions.

So, should we eat salt to our heart’s content?

Pretty much! Our sense of taste has been designed to dictate our nutrient intake. When we don’t have enough sodium, we have a stronger desire to eat salty foods, and vice versa (20). So, we can just listen to what our bodies need and allow that to dictate how much salt we consume.

In other words, salt to taste!

If you’re worried about your blood pressure, then make sure you’re getting enough potassium and magnesium. Reducing sodium intake may drop your blood pressure a few points, but it doesn’t translate to better cardiovascular health.

 

References

Are You Still Restricting Salt?

I was planning on writing about the current salt and sodium recommendations and the lack of solid research supporting them, but I realized that there are already enough comprehensive articles written about that (like this one). Instead, I’ll quickly summarize the absurdity of the current sodium recommendations and focus on the problems caused by restricting salt.

 

Some Ridiculous Guidelines

The current Dietary Guidelines for Americans recommend that we consume less than 2,300 mg sodium per day and less than 1,500 mg sodium for individuals with high blood pressure (1), the World Health Organization recommends that we consume less than 2,000 mg sodium per day (2), and the American Heart Association recommends an ideal limit of no more than 1,500 mg sodium per day for most adults (3).

These recommendations are aimed at reducing hypertension and cardiovascular disease. However, they’re at odds with much of the research, which shows that the current sodium recommendations are between 2 and 4 times lower than what is ideal for cardiovascular health and health in general.

Sodium intakes of 4,000-6,000 mg per day are associated with the lowest risk of cardiovascular death and hospitalization for congestive heart failure (4) while consuming under 2,300 mg sodium per day is associated with increased cardiovascular disease mortality and all-cause mortality (5). And, even consuming less than 3,600 mg per day is associated with greater cardiovascular disease mortality (6).

 

Sodium, the (Almost) Perfect Scapegoat

Ridiculous recommendations aside, sodium is an extraordinarily important mineral that has been wrongly blamed for causing hypertension and cardiovascular disease. This blame comes primarily from sodium’s ability to attract water.

When we consume sodium, the amount of sodium in our blood increases, which increases our blood volume because sodium attracts water.

Our blood pressure is a function of the volume of blood in circulation and the constriction or relaxation of our blood vessels. When our blood volume increases or blood vessels constrict, our blood pressure increases, and vice versa.

So, it’s assumed that increasing sodium consumption increases blood pressure by increasing the blood volume. It’s then assumed that this high blood pressure leads to cardiovascular disease. By the same line of thinking, sodium is blamed for increasing swelling, bloating, and water retention due to its attraction for water.

But, like the “calories-in versus calories-out” model of fat loss, these ideas are based on oversimplified models of the human body that ignore that we adapt to our environments.

When the blood volume is increased from increased salt consumption, our bodies adapt by increasing the amount of sodium they excrete and relaxing our blood vessels. This allows us to maintain a relatively steady blood pressure, while also allowing for optimal blood flow, mineral balance, and energy production. This is easier to explain by describing what happens when we don’t consume enough sodium.

 

What Happens When We Don’t Consume Enough Salt?

Contrary to the mainstream ideas, a low salt intake actually contributes to poor cardiovascular health and swelling and bloating.

When we reduce our salt intake, the amount of sodium in the blood is reduced, which causes an immediate reduction in blood volume and blood pressure. This is why reducing salt intake is suggested for reducing high blood pressure.

But it doesn’t end there.

Maintaining adequate blood pressure is extremely important for transporting nutrients and waste throughout our bodies. So, when our blood pressure is acutely reduced, our stress systems are activated in response (7).

Our stress systems constrict our blood vessels and release the stress hormone aldosterone, which reduces the amount of sodium that we excrete in our kidneys, allowing us to maintain higher sodium (and water) levels in our blood (8). This keeps our blood volume and blood pressure at the levels needed to transport nutrients and waste throughout the body.

But, while this balancing act allows us to maintain blood volume and blood pressure in the short term, it comes at a cost: the sodium we would normally excrete in our kidneys is replaced with potassium and magnesium (9). This means that when we reduce our salt consumption, we lose greater amounts of potassium and magnesium.

Like other adaptive processes, this isn’t a problem in acute situations. But when continued chronically, losing potassium and magnesium can contribute to high blood pressure and inhibit our bodies’ ability to produce energy.

 

Sodium, Swelling, and Energy Production

Potassium and magnesium are balanced with sodium in the cellular environment. Potassium and magnesium are housed within our cells, while sodium remains outside of the cell. This also keeps water outside of the cells (with sodium), which is an important feature of a healthy cell.

When we lose potassium and magnesium due to a low sodium intake, there is less potassium and magnesium in our cells. This then allows more sodium to enter the cell, bringing water with it, which causes the cell to swell (10). The increase in aldosterone due to a low sodium intake also contributes to this cell swelling (11, 12, 13).

This swelling is a real problem – a swollen cell can’t properly produce or use energy (14). Not only is this disastrous for our metabolism, which lies at the foundation of our health, but it can also contribute to cardiovascular problems!

When the cells in our blood vessels swell due to their lack of potassium and magnesium, it inhibits their ability to relax and causes our blood vessels to constrict (like a swollen muscle after working out) (15, 16, 17). This helps to make up for the reduced blood volume from less salt consumption, but also restricts blood flow throughout our bodies and can cause other cardiovascular problems.

In other words, when we eat less salt, our blood pressure is maintained via our stress systems. But, when this occurs over time, we lose potassium and magnesium, leading to cell swelling that inhibits energy production and can cause cardiovascular problems.

 

How Much Salt Should We Eat?

Eating too little salt increases stress, reduces the metabolism, and can lead to cardiovascular problems in the long-term (7, 18, 19).

On the other hand, consuming enough salt allows for optimal energy production, adequate blood volume, reduced swelling and bloating, and sparing of potassium and magnesium. This allows for proper metabolic function, cardiovascular function, and really all other functions.

So, should we eat salt to our heart’s content?

Pretty much! Our sense of taste has been designed to dictate our nutrient intake. When we don’t have enough sodium, we have a stronger desire to eat salty foods, and vice versa (20). So, we can just listen to what our bodies need and allow that to dictate how much salt we consume.

In other words, salt to taste!

If you’re worried about your blood pressure, then make sure you’re getting enough potassium and magnesium. Reducing sodium intake may drop your blood pressure a few points, but it doesn’t translate to better cardiovascular health.

 

References

Are You Still Restricting Salt?

I was planning on writing about the current salt and sodium recommendations and the lack of solid research supporting them, but I realized that there are already enough comprehensive articles written about that (like this one). Instead, I’ll quickly summarize the absurdity of the current sodium recommendations and focus on the problems caused by restricting salt.

 

Some Ridiculous Guidelines

The current Dietary Guidelines for Americans recommend that we consume less than 2,300 mg sodium per day and less than 1,500 mg sodium for individuals with high blood pressure (1), the World Health Organization recommends that we consume less than 2,000 mg sodium per day (2), and the American Heart Association recommends an ideal limit of no more than 1,500 mg sodium per day for most adults (3).

These recommendations are aimed at reducing hypertension and cardiovascular disease. However, they’re at odds with much of the research, which shows that the current sodium recommendations are between 2 and 4 times lower than what is ideal for cardiovascular health and health in general.

Sodium intakes of 4,000-6,000 mg per day are associated with the lowest risk of cardiovascular death and hospitalization for congestive heart failure (4) while consuming under 2,300 mg sodium per day is associated with increased cardiovascular disease mortality and all-cause mortality (5). And, even consuming less than 3,600 mg per day is associated with greater cardiovascular disease mortality (6).

 

Sodium, the (Almost) Perfect Scapegoat

Ridiculous recommendations aside, sodium is an extraordinarily important mineral that has been wrongly blamed for causing hypertension and cardiovascular disease. This blame comes primarily from sodium’s ability to attract water.

When we consume sodium, the amount of sodium in our blood increases, which increases our blood volume because sodium attracts water.

Our blood pressure is a function of the volume of blood in circulation and the constriction or relaxation of our blood vessels. When our blood volume increases or blood vessels constrict, our blood pressure increases, and vice versa.

So, it’s assumed that increasing sodium consumption increases blood pressure by increasing the blood volume. It’s then assumed that this high blood pressure leads to cardiovascular disease. By the same line of thinking, sodium is blamed for increasing swelling, bloating, and water retention due to its attraction for water.

But, like the “calories-in versus calories-out” model of fat loss, these ideas are based on oversimplified models of the human body that ignore that we adapt to our environments.

When the blood volume is increased from increased salt consumption, our bodies adapt by increasing the amount of sodium they excrete and relaxing our blood vessels. This allows us to maintain a relatively steady blood pressure, while also allowing for optimal blood flow, mineral balance, and energy production. This is easier to explain by describing what happens when we don’t consume enough sodium.

 

What Happens When We Don’t Consume Enough Salt?

Contrary to the mainstream ideas, a low salt intake actually contributes to poor cardiovascular health and swelling and bloating.

When we reduce our salt intake, the amount of sodium in the blood is reduced, which causes an immediate reduction in blood volume and blood pressure. This is why reducing salt intake is suggested for reducing high blood pressure.

But it doesn’t end there.

Maintaining adequate blood pressure is extremely important for transporting nutrients and waste throughout our bodies. So, when our blood pressure is acutely reduced, our stress systems are activated in response (7).

Our stress systems constrict our blood vessels and release the stress hormone aldosterone, which reduces the amount of sodium that we excrete in our kidneys, allowing us to maintain higher sodium (and water) levels in our blood (8). This keeps our blood volume and blood pressure at the levels needed to transport nutrients and waste throughout the body.

But, while this balancing act allows us to maintain blood volume and blood pressure in the short term, it comes at a cost: the sodium we would normally excrete in our kidneys is replaced with potassium and magnesium (9). This means that when we reduce our salt consumption, we lose greater amounts of potassium and magnesium.

Like other adaptive processes, this isn’t a problem in acute situations. But when continued chronically, losing potassium and magnesium can contribute to high blood pressure and inhibit our bodies’ ability to produce energy.

 

Sodium, Swelling, and Energy Production

Potassium and magnesium are balanced with sodium in the cellular environment. Potassium and magnesium are housed within our cells, while sodium remains outside of the cell. This also keeps water outside of the cells (with sodium), which is an important feature of a healthy cell.

When we lose potassium and magnesium due to a low sodium intake, there is less potassium and magnesium in our cells. This then allows more sodium to enter the cell, bringing water with it, which causes the cell to swell (10). The increase in aldosterone due to a low sodium intake also contributes to this cell swelling (11, 12, 13).

This swelling is a real problem – a swollen cell can’t properly produce or use energy (14). Not only is this disastrous for our metabolism, which lies at the foundation of our health, but it can also contribute to cardiovascular problems!

When the cells in our blood vessels swell due to their lack of potassium and magnesium, it inhibits their ability to relax and causes our blood vessels to constrict (like a swollen muscle after working out) (15, 16, 17). This helps to make up for the reduced blood volume from less salt consumption, but also restricts blood flow throughout our bodies and can cause other cardiovascular problems.

In other words, when we eat less salt, our blood pressure is maintained via our stress systems. But, when this occurs over time, we lose potassium and magnesium, leading to cell swelling that inhibits energy production and can cause cardiovascular problems.

 

How Much Salt Should We Eat?

Eating too little salt increases stress, reduces the metabolism, and can lead to cardiovascular problems in the long-term (7, 18, 19).

On the other hand, consuming enough salt allows for optimal energy production, adequate blood volume, reduced swelling and bloating, and sparing of potassium and magnesium. This allows for proper metabolic function, cardiovascular function, and really all other functions.

So, should we eat salt to our heart’s content?

Pretty much! Our sense of taste has been designed to dictate our nutrient intake. When we don’t have enough sodium, we have a stronger desire to eat salty foods, and vice versa (20). So, we can just listen to what our bodies need and allow that to dictate how much salt we consume.

In other words, salt to taste!

If you’re worried about your blood pressure, then make sure you’re getting enough potassium and magnesium. Reducing sodium intake may drop your blood pressure a few points, but it doesn’t translate to better cardiovascular health.

 

References

Are You Still Restricting Salt?

I was planning on writing about the current salt and sodium recommendations and the lack of solid research supporting them, but I realized that there are already enough comprehensive articles written about that (like this one). Instead, I’ll quickly summarize the absurdity of the current sodium recommendations and focus on the problems caused by restricting salt.

 

Some Ridiculous Guidelines

The current Dietary Guidelines for Americans recommend that we consume less than 2,300 mg sodium per day and less than 1,500 mg sodium for individuals with high blood pressure (1), the World Health Organization recommends that we consume less than 2,000 mg sodium per day (2), and the American Heart Association recommends an ideal limit of no more than 1,500 mg sodium per day for most adults (3).

These recommendations are aimed at reducing hypertension and cardiovascular disease. However, they’re at odds with much of the research, which shows that the current sodium recommendations are between 2 and 4 times lower than what is ideal for cardiovascular health and health in general.

Sodium intakes of 4,000-6,000 mg per day are associated with the lowest risk of cardiovascular death and hospitalization for congestive heart failure (4) while consuming under 2,300 mg sodium per day is associated with increased cardiovascular disease mortality and all-cause mortality (5). And, even consuming less than 3,600 mg per day is associated with greater cardiovascular disease mortality (6).

 

Sodium, the (Almost) Perfect Scapegoat

Ridiculous recommendations aside, sodium is an extraordinarily important mineral that has been wrongly blamed for causing hypertension and cardiovascular disease. This blame comes primarily from sodium’s ability to attract water.

When we consume sodium, the amount of sodium in our blood increases, which increases our blood volume because sodium attracts water.

Our blood pressure is a function of the volume of blood in circulation and the constriction or relaxation of our blood vessels. When our blood volume increases or blood vessels constrict, our blood pressure increases, and vice versa.

So, it’s assumed that increasing sodium consumption increases blood pressure by increasing the blood volume. It’s then assumed that this high blood pressure leads to cardiovascular disease. By the same line of thinking, sodium is blamed for increasing swelling, bloating, and water retention due to its attraction for water.

But, like the “calories-in versus calories-out” model of fat loss, these ideas are based on oversimplified models of the human body that ignore that we adapt to our environments.

When the blood volume is increased from increased salt consumption, our bodies adapt by increasing the amount of sodium they excrete and relaxing our blood vessels. This allows us to maintain a relatively steady blood pressure, while also allowing for optimal blood flow, mineral balance, and energy production. This is easier to explain by describing what happens when we don’t consume enough sodium.

 

What Happens When We Don’t Consume Enough Salt?

Contrary to the mainstream ideas, a low salt intake actually contributes to poor cardiovascular health and swelling and bloating.

When we reduce our salt intake, the amount of sodium in the blood is reduced, which causes an immediate reduction in blood volume and blood pressure. This is why reducing salt intake is suggested for reducing high blood pressure.

But it doesn’t end there.

Maintaining adequate blood pressure is extremely important for transporting nutrients and waste throughout our bodies. So, when our blood pressure is acutely reduced, our stress systems are activated in response (7).

Our stress systems constrict our blood vessels and release the stress hormone aldosterone, which reduces the amount of sodium that we excrete in our kidneys, allowing us to maintain higher sodium (and water) levels in our blood (8). This keeps our blood volume and blood pressure at the levels needed to transport nutrients and waste throughout the body.

But, while this balancing act allows us to maintain blood volume and blood pressure in the short term, it comes at a cost: the sodium we would normally excrete in our kidneys is replaced with potassium and magnesium (9). This means that when we reduce our salt consumption, we lose greater amounts of potassium and magnesium.

Like other adaptive processes, this isn’t a problem in acute situations. But when continued chronically, losing potassium and magnesium can contribute to high blood pressure and inhibit our bodies’ ability to produce energy.

 

Sodium, Swelling, and Energy Production

Potassium and magnesium are balanced with sodium in the cellular environment. Potassium and magnesium are housed within our cells, while sodium remains outside of the cell. This also keeps water outside of the cells (with sodium), which is an important feature of a healthy cell.

When we lose potassium and magnesium due to a low sodium intake, there is less potassium and magnesium in our cells. This then allows more sodium to enter the cell, bringing water with it, which causes the cell to swell (10). The increase in aldosterone due to a low sodium intake also contributes to this cell swelling (11, 12, 13).

This swelling is a real problem – a swollen cell can’t properly produce or use energy (14). Not only is this disastrous for our metabolism, which lies at the foundation of our health, but it can also contribute to cardiovascular problems!

When the cells in our blood vessels swell due to their lack of potassium and magnesium, it inhibits their ability to relax and causes our blood vessels to constrict (like a swollen muscle after working out) (15, 16, 17). This helps to make up for the reduced blood volume from less salt consumption, but also restricts blood flow throughout our bodies and can cause other cardiovascular problems.

In other words, when we eat less salt, our blood pressure is maintained via our stress systems. But, when this occurs over time, we lose potassium and magnesium, leading to cell swelling that inhibits energy production and can cause cardiovascular problems.

 

How Much Salt Should We Eat?

Eating too little salt increases stress, reduces the metabolism, and can lead to cardiovascular problems in the long-term (7, 18, 19).

On the other hand, consuming enough salt allows for optimal energy production, adequate blood volume, reduced swelling and bloating, and sparing of potassium and magnesium. This allows for proper metabolic function, cardiovascular function, and really all other functions.

So, should we eat salt to our heart’s content?

Pretty much! Our sense of taste has been designed to dictate our nutrient intake. When we don’t have enough sodium, we have a stronger desire to eat salty foods, and vice versa (20). So, we can just listen to what our bodies need and allow that to dictate how much salt we consume.

In other words, salt to taste!

If you’re worried about your blood pressure, then make sure you’re getting enough potassium and magnesium. Reducing sodium intake may drop your blood pressure a few points, but it doesn’t translate to better cardiovascular health.

 

References

Are You Still Restricting Salt?

I was planning on writing about the current salt and sodium recommendations and the lack of solid research supporting them, but I realized that there are already enough comprehensive articles written about that (like this one). Instead, I’ll quickly summarize the absurdity of the current sodium recommendations and focus on the problems caused by restricting salt.

 

Some Ridiculous Guidelines

The current Dietary Guidelines for Americans recommend that we consume less than 2,300 mg sodium per day and less than 1,500 mg sodium for individuals with high blood pressure (1), the World Health Organization recommends that we consume less than 2,000 mg sodium per day (2), and the American Heart Association recommends an ideal limit of no more than 1,500 mg sodium per day for most adults (3).

These recommendations are aimed at reducing hypertension and cardiovascular disease. However, they’re at odds with much of the research, which shows that the current sodium recommendations are between 2 and 4 times lower than what is ideal for cardiovascular health and health in general.

Sodium intakes of 4,000-6,000 mg per day are associated with the lowest risk of cardiovascular death and hospitalization for congestive heart failure (4) while consuming under 2,300 mg sodium per day is associated with increased cardiovascular disease mortality and all-cause mortality (5). And, even consuming less than 3,600 mg per day is associated with greater cardiovascular disease mortality (6).

 

Sodium, the (Almost) Perfect Scapegoat

Ridiculous recommendations aside, sodium is an extraordinarily important mineral that has been wrongly blamed for causing hypertension and cardiovascular disease. This blame comes primarily from sodium’s ability to attract water.

When we consume sodium, the amount of sodium in our blood increases, which increases our blood volume because sodium attracts water.

Our blood pressure is a function of the volume of blood in circulation and the constriction or relaxation of our blood vessels. When our blood volume increases or blood vessels constrict, our blood pressure increases, and vice versa.

So, it’s assumed that increasing sodium consumption increases blood pressure by increasing the blood volume. It’s then assumed that this high blood pressure leads to cardiovascular disease. By the same line of thinking, sodium is blamed for increasing swelling, bloating, and water retention due to its attraction for water.

But, like the “calories-in versus calories-out” model of fat loss, these ideas are based on oversimplified models of the human body that ignore that we adapt to our environments.

When the blood volume is increased from increased salt consumption, our bodies adapt by increasing the amount of sodium they excrete and relaxing our blood vessels. This allows us to maintain a relatively steady blood pressure, while also allowing for optimal blood flow, mineral balance, and energy production. This is easier to explain by describing what happens when we don’t consume enough sodium.

 

What Happens When We Don’t Consume Enough Salt?

Contrary to the mainstream ideas, a low salt intake actually contributes to poor cardiovascular health and swelling and bloating.

When we reduce our salt intake, the amount of sodium in the blood is reduced, which causes an immediate reduction in blood volume and blood pressure. This is why reducing salt intake is suggested for reducing high blood pressure.

But it doesn’t end there.

Maintaining adequate blood pressure is extremely important for transporting nutrients and waste throughout our bodies. So, when our blood pressure is acutely reduced, our stress systems are activated in response (7).

Our stress systems constrict our blood vessels and release the stress hormone aldosterone, which reduces the amount of sodium that we excrete in our kidneys, allowing us to maintain higher sodium (and water) levels in our blood (8). This keeps our blood volume and blood pressure at the levels needed to transport nutrients and waste throughout the body.

But, while this balancing act allows us to maintain blood volume and blood pressure in the short term, it comes at a cost: the sodium we would normally excrete in our kidneys is replaced with potassium and magnesium (9). This means that when we reduce our salt consumption, we lose greater amounts of potassium and magnesium.

Like other adaptive processes, this isn’t a problem in acute situations. But when continued chronically, losing potassium and magnesium can contribute to high blood pressure and inhibit our bodies’ ability to produce energy.

 

Sodium, Swelling, and Energy Production

Potassium and magnesium are balanced with sodium in the cellular environment. Potassium and magnesium are housed within our cells, while sodium remains outside of the cell. This also keeps water outside of the cells (with sodium), which is an important feature of a healthy cell.

When we lose potassium and magnesium due to a low sodium intake, there is less potassium and magnesium in our cells. This then allows more sodium to enter the cell, bringing water with it, which causes the cell to swell (10). The increase in aldosterone due to a low sodium intake also contributes to this cell swelling (11, 12, 13).

This swelling is a real problem – a swollen cell can’t properly produce or use energy (14). Not only is this disastrous for our metabolism, which lies at the foundation of our health, but it can also contribute to cardiovascular problems!

When the cells in our blood vessels swell due to their lack of potassium and magnesium, it inhibits their ability to relax and causes our blood vessels to constrict (like a swollen muscle after working out) (15, 16, 17). This helps to make up for the reduced blood volume from less salt consumption, but also restricts blood flow throughout our bodies and can cause other cardiovascular problems.

In other words, when we eat less salt, our blood pressure is maintained via our stress systems. But, when this occurs over time, we lose potassium and magnesium, leading to cell swelling that inhibits energy production and can cause cardiovascular problems.

 

How Much Salt Should We Eat?

Eating too little salt increases stress, reduces the metabolism, and can lead to cardiovascular problems in the long-term (7, 18, 19).

On the other hand, consuming enough salt allows for optimal energy production, adequate blood volume, reduced swelling and bloating, and sparing of potassium and magnesium. This allows for proper metabolic function, cardiovascular function, and really all other functions.

So, should we eat salt to our heart’s content?

Pretty much! Our sense of taste has been designed to dictate our nutrient intake. When we don’t have enough sodium, we have a stronger desire to eat salty foods, and vice versa (20). So, we can just listen to what our bodies need and allow that to dictate how much salt we consume.

In other words, salt to taste!

If you’re worried about your blood pressure, then make sure you’re getting enough potassium and magnesium. Reducing sodium intake may drop your blood pressure a few points, but it doesn’t translate to better cardiovascular health.

 

References

Are You Still Restricting Salt?

I was planning on writing about the current salt and sodium recommendations and the lack of solid research supporting them, but I realized that there are already enough comprehensive articles written about that (like this one). Instead, I’ll quickly summarize the absurdity of the current sodium recommendations and focus on the problems caused by restricting salt.

 

Some Ridiculous Guidelines

The current Dietary Guidelines for Americans recommend that we consume less than 2,300 mg sodium per day and less than 1,500 mg sodium for individuals with high blood pressure (1), the World Health Organization recommends that we consume less than 2,000 mg sodium per day (2), and the American Heart Association recommends an ideal limit of no more than 1,500 mg sodium per day for most adults (3).

These recommendations are aimed at reducing hypertension and cardiovascular disease. However, they’re at odds with much of the research, which shows that the current sodium recommendations are between 2 and 4 times lower than what is ideal for cardiovascular health and health in general.

Sodium intakes of 4,000-6,000 mg per day are associated with the lowest risk of cardiovascular death and hospitalization for congestive heart failure (4) while consuming under 2,300 mg sodium per day is associated with increased cardiovascular disease mortality and all-cause mortality (5). And, even consuming less than 3,600 mg per day is associated with greater cardiovascular disease mortality (6).

 

Sodium, the (Almost) Perfect Scapegoat

Ridiculous recommendations aside, sodium is an extraordinarily important mineral that has been wrongly blamed for causing hypertension and cardiovascular disease. This blame comes primarily from sodium’s ability to attract water.

When we consume sodium, the amount of sodium in our blood increases, which increases our blood volume because sodium attracts water.

Our blood pressure is a function of the volume of blood in circulation and the constriction or relaxation of our blood vessels. When our blood volume increases or blood vessels constrict, our blood pressure increases, and vice versa.

So, it’s assumed that increasing sodium consumption increases blood pressure by increasing the blood volume. It’s then assumed that this high blood pressure leads to cardiovascular disease. By the same line of thinking, sodium is blamed for increasing swelling, bloating, and water retention due to its attraction for water.

But, like the “calories-in versus calories-out” model of fat loss, these ideas are based on oversimplified models of the human body that ignore that we adapt to our environments.

When the blood volume is increased from increased salt consumption, our bodies adapt by increasing the amount of sodium they excrete and relaxing our blood vessels. This allows us to maintain a relatively steady blood pressure, while also allowing for optimal blood flow, mineral balance, and energy production. This is easier to explain by describing what happens when we don’t consume enough sodium.

 

What Happens When We Don’t Consume Enough Salt?

Contrary to the mainstream ideas, a low salt intake actually contributes to poor cardiovascular health and swelling and bloating.

When we reduce our salt intake, the amount of sodium in the blood is reduced, which causes an immediate reduction in blood volume and blood pressure. This is why reducing salt intake is suggested for reducing high blood pressure.

But it doesn’t end there.

Maintaining adequate blood pressure is extremely important for transporting nutrients and waste throughout our bodies. So, when our blood pressure is acutely reduced, our stress systems are activated in response (7).

Our stress systems constrict our blood vessels and release the stress hormone aldosterone, which reduces the amount of sodium that we excrete in our kidneys, allowing us to maintain higher sodium (and water) levels in our blood (8). This keeps our blood volume and blood pressure at the levels needed to transport nutrients and waste throughout the body.

But, while this balancing act allows us to maintain blood volume and blood pressure in the short term, it comes at a cost: the sodium we would normally excrete in our kidneys is replaced with potassium and magnesium (9). This means that when we reduce our salt consumption, we lose greater amounts of potassium and magnesium.

Like other adaptive processes, this isn’t a problem in acute situations. But when continued chronically, losing potassium and magnesium can contribute to high blood pressure and inhibit our bodies’ ability to produce energy.

 

Sodium, Swelling, and Energy Production

Potassium and magnesium are balanced with sodium in the cellular environment. Potassium and magnesium are housed within our cells, while sodium remains outside of the cell. This also keeps water outside of the cells (with sodium), which is an important feature of a healthy cell.

When we lose potassium and magnesium due to a low sodium intake, there is less potassium and magnesium in our cells. This then allows more sodium to enter the cell, bringing water with it, which causes the cell to swell (10). The increase in aldosterone due to a low sodium intake also contributes to this cell swelling (11, 12, 13).

This swelling is a real problem – a swollen cell can’t properly produce or use energy (14). Not only is this disastrous for our metabolism, which lies at the foundation of our health, but it can also contribute to cardiovascular problems!

When the cells in our blood vessels swell due to their lack of potassium and magnesium, it inhibits their ability to relax and causes our blood vessels to constrict (like a swollen muscle after working out) (15, 16, 17). This helps to make up for the reduced blood volume from less salt consumption, but also restricts blood flow throughout our bodies and can cause other cardiovascular problems.

In other words, when we eat less salt, our blood pressure is maintained via our stress systems. But, when this occurs over time, we lose potassium and magnesium, leading to cell swelling that inhibits energy production and can cause cardiovascular problems.

 

How Much Salt Should We Eat?

Eating too little salt increases stress, reduces the metabolism, and can lead to cardiovascular problems in the long-term (7, 18, 19).

On the other hand, consuming enough salt allows for optimal energy production, adequate blood volume, reduced swelling and bloating, and sparing of potassium and magnesium. This allows for proper metabolic function, cardiovascular function, and really all other functions.

So, should we eat salt to our heart’s content?

Pretty much! Our sense of taste has been designed to dictate our nutrient intake. When we don’t have enough sodium, we have a stronger desire to eat salty foods, and vice versa (20). So, we can just listen to what our bodies need and allow that to dictate how much salt we consume.

In other words, salt to taste!

If you’re worried about your blood pressure, then make sure you’re getting enough potassium and magnesium. Reducing sodium intake may drop your blood pressure a few points, but it doesn’t translate to better cardiovascular health.

 

References

Are You Still Restricting Salt?

I was planning on writing about the current salt and sodium recommendations and the lack of solid research supporting them, but I realized that there are already enough comprehensive articles written about that (like this one). Instead, I’ll quickly summarize the absurdity of the current sodium recommendations and focus on the problems caused by restricting salt.

 

Some Ridiculous Guidelines

The current Dietary Guidelines for Americans recommend that we consume less than 2,300 mg sodium per day and less than 1,500 mg sodium for individuals with high blood pressure (1), the World Health Organization recommends that we consume less than 2,000 mg sodium per day (2), and the American Heart Association recommends an ideal limit of no more than 1,500 mg sodium per day for most adults (3).

These recommendations are aimed at reducing hypertension and cardiovascular disease. However, they’re at odds with much of the research, which shows that the current sodium recommendations are between 2 and 4 times lower than what is ideal for cardiovascular health and health in general.

Sodium intakes of 4,000-6,000 mg per day are associated with the lowest risk of cardiovascular death and hospitalization for congestive heart failure (4) while consuming under 2,300 mg sodium per day is associated with increased cardiovascular disease mortality and all-cause mortality (5). And, even consuming less than 3,600 mg per day is associated with greater cardiovascular disease mortality (6).

 

Sodium, the (Almost) Perfect Scapegoat

Ridiculous recommendations aside, sodium is an extraordinarily important mineral that has been wrongly blamed for causing hypertension and cardiovascular disease. This blame comes primarily from sodium’s ability to attract water.

When we consume sodium, the amount of sodium in our blood increases, which increases our blood volume because sodium attracts water.

Our blood pressure is a function of the volume of blood in circulation and the constriction or relaxation of our blood vessels. When our blood volume increases or blood vessels constrict, our blood pressure increases, and vice versa.

So, it’s assumed that increasing sodium consumption increases blood pressure by increasing the blood volume. It’s then assumed that this high blood pressure leads to cardiovascular disease. By the same line of thinking, sodium is blamed for increasing swelling, bloating, and water retention due to its attraction for water.

But, like the “calories-in versus calories-out” model of fat loss, these ideas are based on oversimplified models of the human body that ignore that we adapt to our environments.

When the blood volume is increased from increased salt consumption, our bodies adapt by increasing the amount of sodium they excrete and relaxing our blood vessels. This allows us to maintain a relatively steady blood pressure, while also allowing for optimal blood flow, mineral balance, and energy production. This is easier to explain by describing what happens when we don’t consume enough sodium.

 

What Happens When We Don’t Consume Enough Salt?

Contrary to the mainstream ideas, a low salt intake actually contributes to poor cardiovascular health and swelling and bloating.

When we reduce our salt intake, the amount of sodium in the blood is reduced, which causes an immediate reduction in blood volume and blood pressure. This is why reducing salt intake is suggested for reducing high blood pressure.

But it doesn’t end there.

Maintaining adequate blood pressure is extremely important for transporting nutrients and waste throughout our bodies. So, when our blood pressure is acutely reduced, our stress systems are activated in response (7).

Our stress systems constrict our blood vessels and release the stress hormone aldosterone, which reduces the amount of sodium that we excrete in our kidneys, allowing us to maintain higher sodium (and water) levels in our blood (8). This keeps our blood volume and blood pressure at the levels needed to transport nutrients and waste throughout the body.

But, while this balancing act allows us to maintain blood volume and blood pressure in the short term, it comes at a cost: the sodium we would normally excrete in our kidneys is replaced with potassium and magnesium (9). This means that when we reduce our salt consumption, we lose greater amounts of potassium and magnesium.

Like other adaptive processes, this isn’t a problem in acute situations. But when continued chronically, losing potassium and magnesium can contribute to high blood pressure and inhibit our bodies’ ability to produce energy.

 

Sodium, Swelling, and Energy Production

Potassium and magnesium are balanced with sodium in the cellular environment. Potassium and magnesium are housed within our cells, while sodium remains outside of the cell. This also keeps water outside of the cells (with sodium), which is an important feature of a healthy cell.

When we lose potassium and magnesium due to a low sodium intake, there is less potassium and magnesium in our cells. This then allows more sodium to enter the cell, bringing water with it, which causes the cell to swell (10). The increase in aldosterone due to a low sodium intake also contributes to this cell swelling (11, 12, 13).

This swelling is a real problem – a swollen cell can’t properly produce or use energy (14). Not only is this disastrous for our metabolism, which lies at the foundation of our health, but it can also contribute to cardiovascular problems!

When the cells in our blood vessels swell due to their lack of potassium and magnesium, it inhibits their ability to relax and causes our blood vessels to constrict (like a swollen muscle after working out) (15, 16, 17). This helps to make up for the reduced blood volume from less salt consumption, but also restricts blood flow throughout our bodies and can cause other cardiovascular problems.

In other words, when we eat less salt, our blood pressure is maintained via our stress systems. But, when this occurs over time, we lose potassium and magnesium, leading to cell swelling that inhibits energy production and can cause cardiovascular problems.

 

How Much Salt Should We Eat?

Eating too little salt increases stress, reduces the metabolism, and can lead to cardiovascular problems in the long-term (7, 18, 19).

On the other hand, consuming enough salt allows for optimal energy production, adequate blood volume, reduced swelling and bloating, and sparing of potassium and magnesium. This allows for proper metabolic function, cardiovascular function, and really all other functions.

So, should we eat salt to our heart’s content?

Pretty much! Our sense of taste has been designed to dictate our nutrient intake. When we don’t have enough sodium, we have a stronger desire to eat salty foods, and vice versa (20). So, we can just listen to what our bodies need and allow that to dictate how much salt we consume.

In other words, salt to taste!

If you’re worried about your blood pressure, then make sure you’re getting enough potassium and magnesium. Reducing sodium intake may drop your blood pressure a few points, but it doesn’t translate to better cardiovascular health.

 

References

Are You Still Restricting Salt?

I was planning on writing about the current salt and sodium recommendations and the lack of solid research supporting them, but I realized that there are already enough comprehensive articles written about that (like this one). Instead, I’ll quickly summarize the absurdity of the current sodium recommendations and focus on the problems caused by restricting salt.

 

Some Ridiculous Guidelines

The current Dietary Guidelines for Americans recommend that we consume less than 2,300 mg sodium per day and less than 1,500 mg sodium for individuals with high blood pressure (1), the World Health Organization recommends that we consume less than 2,000 mg sodium per day (2), and the American Heart Association recommends an ideal limit of no more than 1,500 mg sodium per day for most adults (3).

These recommendations are aimed at reducing hypertension and cardiovascular disease. However, they’re at odds with much of the research, which shows that the current sodium recommendations are between 2 and 4 times lower than what is ideal for cardiovascular health and health in general.

Sodium intakes of 4,000-6,000 mg per day are associated with the lowest risk of cardiovascular death and hospitalization for congestive heart failure (4) while consuming under 2,300 mg sodium per day is associated with increased cardiovascular disease mortality and all-cause mortality (5). And, even consuming less than 3,600 mg per day is associated with greater cardiovascular disease mortality (6).

 

Sodium, the (Almost) Perfect Scapegoat

Ridiculous recommendations aside, sodium is an extraordinarily important mineral that has been wrongly blamed for causing hypertension and cardiovascular disease. This blame comes primarily from sodium’s ability to attract water.

When we consume sodium, the amount of sodium in our blood increases, which increases our blood volume because sodium attracts water.

Our blood pressure is a function of the volume of blood in circulation and the constriction or relaxation of our blood vessels. When our blood volume increases or blood vessels constrict, our blood pressure increases, and vice versa.

So, it’s assumed that increasing sodium consumption increases blood pressure by increasing the blood volume. It’s then assumed that this high blood pressure leads to cardiovascular disease. By the same line of thinking, sodium is blamed for increasing swelling, bloating, and water retention due to its attraction for water.

But, like the “calories-in versus calories-out” model of fat loss, these ideas are based on oversimplified models of the human body that ignore that we adapt to our environments.

When the blood volume is increased from increased salt consumption, our bodies adapt by increasing the amount of sodium they excrete and relaxing our blood vessels. This allows us to maintain a relatively steady blood pressure, while also allowing for optimal blood flow, mineral balance, and energy production. This is easier to explain by describing what happens when we don’t consume enough sodium.

 

What Happens When We Don’t Consume Enough Salt?

Contrary to the mainstream ideas, a low salt intake actually contributes to poor cardiovascular health and swelling and bloating.

When we reduce our salt intake, the amount of sodium in the blood is reduced, which causes an immediate reduction in blood volume and blood pressure. This is why reducing salt intake is suggested for reducing high blood pressure.

But it doesn’t end there.

Maintaining adequate blood pressure is extremely important for transporting nutrients and waste throughout our bodies. So, when our blood pressure is acutely reduced, our stress systems are activated in response (7).

Our stress systems constrict our blood vessels and release the stress hormone aldosterone, which reduces the amount of sodium that we excrete in our kidneys, allowing us to maintain higher sodium (and water) levels in our blood (8). This keeps our blood volume and blood pressure at the levels needed to transport nutrients and waste throughout the body.

But, while this balancing act allows us to maintain blood volume and blood pressure in the short term, it comes at a cost: the sodium we would normally excrete in our kidneys is replaced with potassium and magnesium (9). This means that when we reduce our salt consumption, we lose greater amounts of potassium and magnesium.

Like other adaptive processes, this isn’t a problem in acute situations. But when continued chronically, losing potassium and magnesium can contribute to high blood pressure and inhibit our bodies’ ability to produce energy.

 

Sodium, Swelling, and Energy Production

Potassium and magnesium are balanced with sodium in the cellular environment. Potassium and magnesium are housed within our cells, while sodium remains outside of the cell. This also keeps water outside of the cells (with sodium), which is an important feature of a healthy cell.

When we lose potassium and magnesium due to a low sodium intake, there is less potassium and magnesium in our cells. This then allows more sodium to enter the cell, bringing water with it, which causes the cell to swell (10). The increase in aldosterone due to a low sodium intake also contributes to this cell swelling (11, 12, 13).

This swelling is a real problem – a swollen cell can’t properly produce or use energy (14). Not only is this disastrous for our metabolism, which lies at the foundation of our health, but it can also contribute to cardiovascular problems!

When the cells in our blood vessels swell due to their lack of potassium and magnesium, it inhibits their ability to relax and causes our blood vessels to constrict (like a swollen muscle after working out) (15, 16, 17). This helps to make up for the reduced blood volume from less salt consumption, but also restricts blood flow throughout our bodies and can cause other cardiovascular problems.

In other words, when we eat less salt, our blood pressure is maintained via our stress systems. But, when this occurs over time, we lose potassium and magnesium, leading to cell swelling that inhibits energy production and can cause cardiovascular problems.

 

How Much Salt Should We Eat?

Eating too little salt increases stress, reduces the metabolism, and can lead to cardiovascular problems in the long-term (7, 18, 19).

On the other hand, consuming enough salt allows for optimal energy production, adequate blood volume, reduced swelling and bloating, and sparing of potassium and magnesium. This allows for proper metabolic function, cardiovascular function, and really all other functions.

So, should we eat salt to our heart’s content?

Pretty much! Our sense of taste has been designed to dictate our nutrient intake. When we don’t have enough sodium, we have a stronger desire to eat salty foods, and vice versa (20). So, we can just listen to what our bodies need and allow that to dictate how much salt we consume.

In other words, salt to taste!

If you’re worried about your blood pressure, then make sure you’re getting enough potassium and magnesium. Reducing sodium intake may drop your blood pressure a few points, but it doesn’t translate to better cardiovascular health.

 

References

Are You Still Restricting Salt?

I was planning on writing about the current salt and sodium recommendations and the lack of solid research supporting them, but I realized that there are already enough comprehensive articles written about that (like this one). Instead, I’ll quickly summarize the absurdity of the current sodium recommendations and focus on the problems caused by restricting salt.

 

Some Ridiculous Guidelines

The current Dietary Guidelines for Americans recommend that we consume less than 2,300 mg sodium per day and less than 1,500 mg sodium for individuals with high blood pressure (1), the World Health Organization recommends that we consume less than 2,000 mg sodium per day (2), and the American Heart Association recommends an ideal limit of no more than 1,500 mg sodium per day for most adults (3).

These recommendations are aimed at reducing hypertension and cardiovascular disease. However, they’re at odds with much of the research, which shows that the current sodium recommendations are between 2 and 4 times lower than what is ideal for cardiovascular health and health in general.

Sodium intakes of 4,000-6,000 mg per day are associated with the lowest risk of cardiovascular death and hospitalization for congestive heart failure (4) while consuming under 2,300 mg sodium per day is associated with increased cardiovascular disease mortality and all-cause mortality (5). And, even consuming less than 3,600 mg per day is associated with greater cardiovascular disease mortality (6).

 

Sodium, the (Almost) Perfect Scapegoat

Ridiculous recommendations aside, sodium is an extraordinarily important mineral that has been wrongly blamed for causing hypertension and cardiovascular disease. This blame comes primarily from sodium’s ability to attract water.

When we consume sodium, the amount of sodium in our blood increases, which increases our blood volume because sodium attracts water.

Our blood pressure is a function of the volume of blood in circulation and the constriction or relaxation of our blood vessels. When our blood volume increases or blood vessels constrict, our blood pressure increases, and vice versa.

So, it’s assumed that increasing sodium consumption increases blood pressure by increasing the blood volume. It’s then assumed that this high blood pressure leads to cardiovascular disease. By the same line of thinking, sodium is blamed for increasing swelling, bloating, and water retention due to its attraction for water.

But, like the “calories-in versus calories-out” model of fat loss, these ideas are based on oversimplified models of the human body that ignore that we adapt to our environments.

When the blood volume is increased from increased salt consumption, our bodies adapt by increasing the amount of sodium they excrete and relaxing our blood vessels. This allows us to maintain a relatively steady blood pressure, while also allowing for optimal blood flow, mineral balance, and energy production. This is easier to explain by describing what happens when we don’t consume enough sodium.

 

What Happens When We Don’t Consume Enough Salt?

Contrary to the mainstream ideas, a low salt intake actually contributes to poor cardiovascular health and swelling and bloating.

When we reduce our salt intake, the amount of sodium in the blood is reduced, which causes an immediate reduction in blood volume and blood pressure. This is why reducing salt intake is suggested for reducing high blood pressure.

But it doesn’t end there.

Maintaining adequate blood pressure is extremely important for transporting nutrients and waste throughout our bodies. So, when our blood pressure is acutely reduced, our stress systems are activated in response (7).

Our stress systems constrict our blood vessels and release the stress hormone aldosterone, which reduces the amount of sodium that we excrete in our kidneys, allowing us to maintain higher sodium (and water) levels in our blood (8). This keeps our blood volume and blood pressure at the levels needed to transport nutrients and waste throughout the body.

But, while this balancing act allows us to maintain blood volume and blood pressure in the short term, it comes at a cost: the sodium we would normally excrete in our kidneys is replaced with potassium and magnesium (9). This means that when we reduce our salt consumption, we lose greater amounts of potassium and magnesium.

Like other adaptive processes, this isn’t a problem in acute situations. But when continued chronically, losing potassium and magnesium can contribute to high blood pressure and inhibit our bodies’ ability to produce energy.

 

Sodium, Swelling, and Energy Production

Potassium and magnesium are balanced with sodium in the cellular environment. Potassium and magnesium are housed within our cells, while sodium remains outside of the cell. This also keeps water outside of the cells (with sodium), which is an important feature of a healthy cell.

When we lose potassium and magnesium due to a low sodium intake, there is less potassium and magnesium in our cells. This then allows more sodium to enter the cell, bringing water with it, which causes the cell to swell (10). The increase in aldosterone due to a low sodium intake also contributes to this cell swelling (11, 12, 13).

This swelling is a real problem – a swollen cell can’t properly produce or use energy (14). Not only is this disastrous for our metabolism, which lies at the foundation of our health, but it can also contribute to cardiovascular problems!

When the cells in our blood vessels swell due to their lack of potassium and magnesium, it inhibits their ability to relax and causes our blood vessels to constrict (like a swollen muscle after working out) (15, 16, 17). This helps to make up for the reduced blood volume from less salt consumption, but also restricts blood flow throughout our bodies and can cause other cardiovascular problems.

In other words, when we eat less salt, our blood pressure is maintained via our stress systems. But, when this occurs over time, we lose potassium and magnesium, leading to cell swelling that inhibits energy production and can cause cardiovascular problems.

 

How Much Salt Should We Eat?

Eating too little salt increases stress, reduces the metabolism, and can lead to cardiovascular problems in the long-term (7, 18, 19).

On the other hand, consuming enough salt allows for optimal energy production, adequate blood volume, reduced swelling and bloating, and sparing of potassium and magnesium. This allows for proper metabolic function, cardiovascular function, and really all other functions.

So, should we eat salt to our heart’s content?

Pretty much! Our sense of taste has been designed to dictate our nutrient intake. When we don’t have enough sodium, we have a stronger desire to eat salty foods, and vice versa (20). So, we can just listen to what our bodies need and allow that to dictate how much salt we consume.

In other words, salt to taste!

If you’re worried about your blood pressure, then make sure you’re getting enough potassium and magnesium. Reducing sodium intake may drop your blood pressure a few points, but it doesn’t translate to better cardiovascular health.

 

References

Are You Still Restricting Salt?

I was planning on writing about the current salt and sodium recommendations and the lack of solid research supporting them, but I realized that there are already enough comprehensive articles written about that (like this one). Instead, I’ll quickly summarize the absurdity of the current sodium recommendations and focus on the problems caused by restricting salt.

 

Some Ridiculous Guidelines

The current Dietary Guidelines for Americans recommend that we consume less than 2,300 mg sodium per day and less than 1,500 mg sodium for individuals with high blood pressure (1), the World Health Organization recommends that we consume less than 2,000 mg sodium per day (2), and the American Heart Association recommends an ideal limit of no more than 1,500 mg sodium per day for most adults (3).

These recommendations are aimed at reducing hypertension and cardiovascular disease. However, they’re at odds with much of the research, which shows that the current sodium recommendations are between 2 and 4 times lower than what is ideal for cardiovascular health and health in general.

Sodium intakes of 4,000-6,000 mg per day are associated with the lowest risk of cardiovascular death and hospitalization for congestive heart failure (4) while consuming under 2,300 mg sodium per day is associated with increased cardiovascular disease mortality and all-cause mortality (5). And, even consuming less than 3,600 mg per day is associated with greater cardiovascular disease mortality (6).

 

Sodium, the (Almost) Perfect Scapegoat

Ridiculous recommendations aside, sodium is an extraordinarily important mineral that has been wrongly blamed for causing hypertension and cardiovascular disease. This blame comes primarily from sodium’s ability to attract water.

When we consume sodium, the amount of sodium in our blood increases, which increases our blood volume because sodium attracts water.

Our blood pressure is a function of the volume of blood in circulation and the constriction or relaxation of our blood vessels. When our blood volume increases or blood vessels constrict, our blood pressure increases, and vice versa.

So, it’s assumed that increasing sodium consumption increases blood pressure by increasing the blood volume. It’s then assumed that this high blood pressure leads to cardiovascular disease. By the same line of thinking, sodium is blamed for increasing swelling, bloating, and water retention due to its attraction for water.

But, like the “calories-in versus calories-out” model of fat loss, these ideas are based on oversimplified models of the human body that ignore that we adapt to our environments.

When the blood volume is increased from increased salt consumption, our bodies adapt by increasing the amount of sodium they excrete and relaxing our blood vessels. This allows us to maintain a relatively steady blood pressure, while also allowing for optimal blood flow, mineral balance, and energy production. This is easier to explain by describing what happens when we don’t consume enough sodium.

 

What Happens When We Don’t Consume Enough Salt?

Contrary to the mainstream ideas, a low salt intake actually contributes to poor cardiovascular health and swelling and bloating.

When we reduce our salt intake, the amount of sodium in the blood is reduced, which causes an immediate reduction in blood volume and blood pressure. This is why reducing salt intake is suggested for reducing high blood pressure.

But it doesn’t end there.

Maintaining adequate blood pressure is extremely important for transporting nutrients and waste throughout our bodies. So, when our blood pressure is acutely reduced, our stress systems are activated in response (7).

Our stress systems constrict our blood vessels and release the stress hormone aldosterone, which reduces the amount of sodium that we excrete in our kidneys, allowing us to maintain higher sodium (and water) levels in our blood (8). This keeps our blood volume and blood pressure at the levels needed to transport nutrients and waste throughout the body.

But, while this balancing act allows us to maintain blood volume and blood pressure in the short term, it comes at a cost: the sodium we would normally excrete in our kidneys is replaced with potassium and magnesium (9). This means that when we reduce our salt consumption, we lose greater amounts of potassium and magnesium.

Like other adaptive processes, this isn’t a problem in acute situations. But when continued chronically, losing potassium and magnesium can contribute to high blood pressure and inhibit our bodies’ ability to produce energy.

 

Sodium, Swelling, and Energy Production

Potassium and magnesium are balanced with sodium in the cellular environment. Potassium and magnesium are housed within our cells, while sodium remains outside of the cell. This also keeps water outside of the cells (with sodium), which is an important feature of a healthy cell.

When we lose potassium and magnesium due to a low sodium intake, there is less potassium and magnesium in our cells. This then allows more sodium to enter the cell, bringing water with it, which causes the cell to swell (10). The increase in aldosterone due to a low sodium intake also contributes to this cell swelling (11, 12, 13).

This swelling is a real problem – a swollen cell can’t properly produce or use energy (14). Not only is this disastrous for our metabolism, which lies at the foundation of our health, but it can also contribute to cardiovascular problems!

When the cells in our blood vessels swell due to their lack of potassium and magnesium, it inhibits their ability to relax and causes our blood vessels to constrict (like a swollen muscle after working out) (15, 16, 17). This helps to make up for the reduced blood volume from less salt consumption, but also restricts blood flow throughout our bodies and can cause other cardiovascular problems.

In other words, when we eat less salt, our blood pressure is maintained via our stress systems. But, when this occurs over time, we lose potassium and magnesium, leading to cell swelling that inhibits energy production and can cause cardiovascular problems.

 

How Much Salt Should We Eat?

Eating too little salt increases stress, reduces the metabolism, and can lead to cardiovascular problems in the long-term (7, 18, 19).

On the other hand, consuming enough salt allows for optimal energy production, adequate blood volume, reduced swelling and bloating, and sparing of potassium and magnesium. This allows for proper metabolic function, cardiovascular function, and really all other functions.

So, should we eat salt to our heart’s content?

Pretty much! Our sense of taste has been designed to dictate our nutrient intake. When we don’t have enough sodium, we have a stronger desire to eat salty foods, and vice versa (20). So, we can just listen to what our bodies need and allow that to dictate how much salt we consume.

In other words, salt to taste!

If you’re worried about your blood pressure, then make sure you’re getting enough potassium and magnesium. Reducing sodium intake may drop your blood pressure a few points, but it doesn’t translate to better cardiovascular health.

 

References